Are We Carrying More Than Previous Generations Did? What modern trauma exposure is doing to our brains, and what genuinely helps.

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A short answer first. Yes, contemporary adults are exposed to more potentially traumatic material than any previous generation, much of it through screens. The neurobiological effects of that exposure are well documented at the individual level. The population-level implications are harder to test directly but are reasonable to infer from the data we do have. The picture is not deterministic. Treatment works. Buffering works. The path through is real and well evidenced.

Quick answer

Contemporary adults face higher cumulative trauma exposure than previous generations, including indirect exposure through media. This produces documented changes in the hippocampus, amygdala, prefrontal cortex, HPA axis, and vagal tone at the individual level. People from high intergenerational trauma backgrounds carry additional load and are more susceptible to the population-level shift. Treatment is effective. Evidence-based options include trauma-focused CBT, cognitive processing therapy, prolonged exposure, EMDR, phase-based treatment for complex PTSD, dialectical behaviour therapy, mindfulness-based interventions, body-based approaches, and MDMA-assisted psychotherapy. The most effective treatment depends on the individual presentation.

Key takeaways

• Mean adverse childhood experience scores have risen from 0.79 for Americans born before 1940 to 2.74 for those born in 1998, with projected scores above 3 for the 2018 birth cohort (Anderson et al., 2023).

• Trauma exposure reliably reduces hippocampal volume, increases amygdala reactivity, reduces prefrontal cortex regulation, dysregulates the HPA axis, and lowers heart rate variability (Teicher et al., 2016; McEwen et al., 2016).

• Indirect screen-based exposure activates the same threat-detection circuitry as direct exposure, with media exposure of 6+ hours daily during the 2013 Boston Marathon bombings producing higher acute stress than direct on-site exposure (Holman, Garfin & Silver, 2014).

• At least one-third of Aboriginal and Torres Strait Islander Australians are affected by intergenerational trauma as descendants of the Stolen Generations (AIHW, 2023). Intergenerational trauma transmits through epigenetic, in utero, attachment, and structural mechanisms.

• First-line evidence-based treatments for PTSD include trauma-focused CBT, cognitive processing therapy, prolonged exposure, and EMDR. For complex PTSD, phase-based treatment is recommended by 84 per cent of expert clinicians (ISTSS expert consensus).

• Buffering structures are individual rather than universal. What regulates one nervous system can dysregulate another. Sensory-sensitive, neurodivergent, attachment-disrupted, and autonomically-compromised individuals require different buffering profiles.

• MDMA-assisted therapy produced PTSD remission in 67 per cent of treated participants in phase 3 trials (Mitchell et al., 2021). The Australian Therapeutic Goods Administration authorised MDMA for PTSD treatment from July 2023.

  
  

The question worth asking

Most adults I see in therapy describe a low-grade hum of activation that they cannot quite turn off. Trouble sleeping. Tension that does not match what is happening on any given day. A scrolling habit that feels compulsive rather than informative. A sense that the world is loud in ways it was not loud before. These are not failures of character or coping. They are predictable responses to a level of exposure that older generations did not face at the same scale or with the same pattern of delivery.

The clinical question is whether this elevated background load actually translates into higher mental health risk than previous generations faced, and if so, what the mechanism is and what we can do about it. Drawing together two recent reviews I prepared (one on generational shifts in trauma exposure, the other on the neurobiology of direct and indirect trauma), this post lays out the evidence and, importantly, what genuinely helps for those who did not have the right level of buffering structures growing up.

Trauma exposure has changed in ways that show up in the data

The World Mental Health Survey Consortium, drawing on close to 69,000 adults across 24 countries, found that around 70 per cent of people report exposure to at least one potentially traumatic event in their lifetime, with 30 per cent reporting four or more (Benjet et al., 2016). Those figures alone are higher than most people assume.

Generational comparisons make the trend clearer. Using United States Behavioral Risk Factor Surveillance System data, Anderson and colleagues (2023) found that mean adverse childhood experience scores rose from 0.79 among Americans born in or before 1940 to 2.74 among Americans born in 1998. The projected score for adults born in 2018 exceeds three. Even allowing for the fact that older cohorts may underreport due to generational norms around stoicism, the magnitude of this rise is unlikely to be a measurement artefact.

Indirect exposure has expanded in a more dramatic way. Where previous generations encountered atrocities through weekly newsreels, daily newspapers, or scheduled evening television, contemporary adults can be exposed to first-person body-camera footage of mass shootings, drone strike footage from active war zones, or live-streamed terror attacks within hours of the events occurring. Forcibly displaced persons globally reached 122 million in 2025, nearly double the figure a decade earlier (UNHCR Global Trends Report, 2025).

The combined effect is that the catchment of potentially traumatic material a typical adult encounters has expanded substantially, even where the rate of direct interpersonal violence in the immediate home environment has declined for some populations.

What this does to the brain

The neurobiology of trauma exposure is one of the most replicable bodies of evidence in psychiatry and clinical neuroscience. Three brain regions show consistent change across studies.

The hippocampus, which supports memory and helps the brain regulate the stress response, shows volume reduction and impaired neurogenesis with chronic exposure (Teicher, Samson, Anderson & Ohashi, 2016). The amygdala, which detects and responds to threat, shows dendritic growth and heightened reactivity. The prefrontal cortex, which provides top-down regulation of the amygdala, shows reduced volume and reduced activity. Connectivity between these regions is disrupted (McEwen, Nasca & Gray, 2016).

Underneath these structural changes sits a set of neurochemical shifts. Hypothalamic-pituitary-adrenal axis dysregulation is the most consistent neuroendocrine finding, with patterns differing by trauma type. Brain-derived neurotrophic factor is suppressed by chronic glucocorticoid exposure. Heart rate variability, which indexes the flexibility of the autonomic nervous system, is reduced. Low-grade systemic inflammation is sustained. Epigenetic modifications to the glucocorticoid receptor gene have been documented in postmortem hippocampal tissue from individuals with histories of childhood abuse (McGowan et al., 2009).

The indirect-exposure parallel

A study published in the Proceedings of the National Academy of Sciences found that more than six daily hours of bombing-related media exposure during the week of the 2013 Boston Marathon bombings was associated with higher acute stress symptoms than direct exposure at the bombing site itself (Holman, Garfin & Silver, 2014). The same threat-detection circuitry activates whether the exposure is in person or on a screen, with the difference that screen exposure is sustained, repeatable, and decoupled from the natural resolution that ends most direct threats.

For neurodivergent adults the picture has an additional layer. Rumball, Happé and Grey (2020) reported probable PTSD rates of 45 per cent for current and 61 per cent for lifetime probable PTSD in trauma-exposed autistic adults, compared with around 4 per cent in the general population. A meta-analysis of close to four million participants found that adverse childhood experiences were significantly associated with subsequent ADHD diagnosis, with an odds ratio of 1.68 (Zhang et al., 2022).

The combined answer

So, are we more at risk than previous generations? The evidence supports a yes, with moderate to high confidence. Cumulative exposure has risen across recent birth cohorts. The neurobiological cascade that follows exposure is well documented at the individual level. The clinical correlates (rising rates of anxiety and depression in young adults, declining adolescent mental health metrics across multiple OECD countries, increased presentations of complex trauma and burnout) are visible in epidemiological data.

The harder claim is what is happening at a population level to our brain chemistry as a society. We do not have generational neuroimaging cohorts. We cannot directly compare the mean amygdala reactivity of Australian adults in 2026 with the mean amygdala reactivity of Australian adults in 1975. The direct test has not been done.

The reasonable inference

The data we do have is solid enough to suggest that if the test were run, we would likely see a measurable shift in the population direction. More exposure inputs, applied to more people, producing the same neurobiological cascade that is reliably observed in exposed individuals, must in aggregate move the population mean. The plausible direction is toward greater sustained sympathetic arousal, lower mean vagal tone, sharper threat-scanning calibration, and chronic low-grade inflammation than the equivalent cohort showed fifty years ago. We are inferring rather than measuring, but the inference is not speculative. It follows from the underlying evidence.

This is what people mean, in non-technical language, when they say the world feels more anxious than it used to feel. The feeling is not an illusion. It has a neurobiological substrate that we can name and, importantly, work with.

Buffering matters, and what counts as buffering is individual

Not every exposed adult develops a disorder, and the difference between those who do and those who do not is partly accounted for by buffering structures. Cohen and Wills (1985), in a foundational paper in Psychological Bulletin, set out the stress-buffering hypothesis, which holds that social support reduces the impact of stressful life events on mental and physical health outcomes. The hypothesis has been supported across decades of subsequent meta-analytic work (Vila, 2021, in Frontiers in Psychology, summarised 23 meta-analyses including more than 1.4 billion participants).

Buffering, in plain language, refers to the structures that help the nervous system return to baseline after activation, that help a person feel safe and connected, and that absorb some of the impact of exposure before it produces lasting change. The conventional list includes secure attachment relationships in childhood, stable housing, predictable income, meaningful work, religious or spiritual community, physical activity, sleep, nature exposure, and intergenerational connection. The list is correct as a starting point but it is also a population-level summary, not an individual prescription.

What counts as buffering varies by individual

In clinical practice the picture is more layered than the textbook list suggests. The same input that buffers one person can drain another. Some examples worth sitting with.

For an extroverted, neurotypical adult, a large social gathering may be genuinely restorative. For an autistic adult or someone with high sensory sensitivity, the same gathering may be a stressor that depletes rather than replenishes. The buffering category for that person might be solo time in a quiet environment, focused interest engagement, or a small number of low-demand relationships rather than broad social contact.

For an adult with secure attachment history, talking with a trusted friend about a difficult event may be regulating. For an adult with developmental trauma and disorganised attachment, the same conversation may activate rather than soothe. The buffering category for that person might be somatic regulation, structured ritual, time with animals, or relationships that have been carefully built over time with explicit safety agreements.

For a person with strong cultural or spiritual practice, ritual and ceremony can be powerful regulators. For someone whose family-of-origin religion was harmful, the same practices may be retraumatising. The buffering category for that person might be a self-chosen meaning-making practice rather than an inherited one.

For an athlete or someone with high baseline cardiovascular fitness, vigorous exercise reliably regulates mood. For a person with chronic fatigue, dysautonomia, hypermobility spectrum conditions, or post-viral illness, the same exercise prescription can trigger crashes that worsen mental health. The buffering category for that person might be gentle movement, paced activity, and explicit attention to autonomic recovery rather than aerobic intensity.

A clinical principle worth holding

Buffering is whatever genuinely helps your particular nervous system return to baseline. It is identified by careful attention to what increases your capacity over time, not by following a generic wellness checklist. Two people with similar trauma histories may need substantially different buffering profiles.

Why some groups carry more of this load to begin with

Not every adult starts from the same baseline. Some people enter adulthood already carrying a stress physiology shaped by what happened to their parents and grandparents. This is not a poetic claim. It is one of the better-evidenced findings in psychiatric epidemiology and developmental science, and it changes the picture of who is most susceptible to the broader shift in brain chemistry that contemporary exposure produces.

Intergenerational trauma refers to the transmission of trauma effects from one generation to the next, even when the descendant has not directly experienced the original event. The mechanisms are multiple and they operate together rather than in isolation. Understanding them matters clinically because the entry point for treatment, and the realistic timeline, look different for someone who is carrying ancestral and family-of-origin load alongside their own current exposure.

The four mechanisms of transmission

The first mechanism is epigenetic. Yehuda and colleagues (2014, 2016, 2018) and Bierer and colleagues (2020), working with adult offspring of Holocaust survivors, have documented altered methylation of the glucocorticoid receptor gene (NR3C1) and the FKBP5 gene, both of which sit at the heart of HPA axis regulation. The methylation patterns in offspring differ from controls in ways that track with parental trauma exposure and parental PTSD status. Mulligan and colleagues (2025), publishing in Scientific Reports, extended this work to three generations of Syrian refugees and identified differentially methylated regions associated with both direct and germline (grandmother-line) exposure to war-related violence, alongside epigenetic age acceleration in children whose mothers were pregnant during war exposure. The evidence in humans is strongest for parent-to-child (F1 to F2) effects and remains more contested beyond that, but the pattern of HPA-axis-relevant methylation changes is now replicated across multiple research groups and populations.

The second mechanism is in utero and perinatal. A mother who is pregnant while highly stressed or traumatised shows altered placental cortisol regulation, with downstream effects on fetal HPA axis programming. This is not epigenetic inheritance in the strict sense, since the developing fetus is directly exposed to maternal stress hormones, but the consequence is similar. The child arrives with a stress system that has been calibrated for a high-threat environment.

The third mechanism is attachment and parenting. Parents who are themselves carrying unresolved trauma frequently parent in ways that pass on dysregulation, often without intending to. The TRANS-GEN study and related research show that maternal childhood maltreatment predicts altered infant cortisol regulation, mediated partly by disoriented or negative-intrusive caregiving (Lyons-Ruth and colleagues, summarised in Pace et al., 2022). Disrupted attachment shapes the developing infant brain, and disrupted infant brains then produce adults who often struggle to provide secure attachment for their own children. The cycle is not inevitable but it is statistically well established.

The fourth mechanism is social and structural. The conditions that produced the original trauma frequently persist across generations. Colonisation, racism, displacement, and systemic disadvantage are not historical events that ended at a particular date. They continue to shape the environments in which descendants are raised, the resources available to them, and the daily stressors they face. A Duke University review (Martin and colleagues, 2025, in Social Science and Medicine) argued that current structural racism explains contemporary Black-White health disparities in the United States more parsimoniously than transgenerational epigenetic inheritance does, and the same logic applies to other groups. The point is not that epigenetics is wrong, since the evidence supports parent-to-child effects, but that ongoing exposure is doing significant work alongside any inherited biological signature.

Who carries this load in the Australian context

In Australia the most clearly affected group is Aboriginal and Torres Strait Islander peoples. The Australian Institute of Health and Welfare estimates that at a minimum one-third of the total Aboriginal and Torres Strait Islander population is affected by intergenerational trauma as descendants of the Stolen Generations (AIHW, 2023). Atkinson (2002), in her foundational text Trauma Trails, set out the framework for understanding the layered impact of dispossession, child removal policies, cultural rupture, and continuing structural disadvantage. Recent population-attributable fraction work in The Lancet Regional Health Western Pacific (Diminic and colleagues, 2024) found that mental disorders account for around 20 per cent of the Aboriginal and Torres Strait Islander health gap, with intergenerational trauma identified as a major upstream driver.

Other groups carrying significant intergenerational load in the Australian community include descendants of Holocaust survivors, refugees from war zones (Vietnamese, Cambodian, former Yugoslavian, Iraqi, Afghani, Sudanese, Syrian, and more recent Ukrainian and Gazan arrivals), descendants of those affected by the Armenian, Cambodian, and Rwandan genocides, and adults from families where cycles of abuse, neglect, or domestic violence have continued across generations. Sangalang and Vang (2017), in a systematic review of refugee family studies, found that more than half of the included studies showed elevated psychological vulnerability in the next generation, including elevated rates of PTSD, mood disorders, and anxiety symptoms.

What this means for susceptibility to the current shift

A person who enters adulthood with an HPA axis that was calibrated by parental or grandparental trauma exposure has, on average, less spare capacity to absorb the current generational increase in exposure. Their amygdala is already more reactive. Their cortisol regulation is already further from optimal. Their vagal tone is on average lower. The buffering structures available to them are often the same ones that have been worn thin by the original trauma (family, culture, community, ritual) or are themselves sources of ongoing harm rather than support.

This is why the same societal-level exposure does not produce the same effect across the population. A young adult from a family with three secure-attachment generations behind them and stable housing, income, and community will experience the increase in trauma exposure that this post has described, and most will adapt. A young adult who is the great-grandchild of Stolen Generations survivors, raised in a community still navigating the consequences of cultural disruption and structural racism, exposed to ongoing discrimination, with attachment relationships shaped by parents who themselves carried unresolved trauma, will experience the same societal-level increase from a starting point that is already substantially further from baseline. The downstream neurobiological effect is greater, not because the exposure was different, but because the susceptibility was different.

Clinical implication

Treatment still works for adults from high intergenerational trauma backgrounds, and the evidence for that is strong. The realistic timeline is often longer. The work frequently needs to be paced more carefully. For First Nations clients in particular, individual therapy alone is rarely sufficient. Healing is more reliably effective when it is collective, culturally grounded, and held by community rather than delivered solely in a one-to-one room. The Atkinson (2002) framework and subsequent Aboriginal community-controlled health service models are explicit about this. A clinician working with an Aboriginal or Torres Strait Islander client carrying intergenerational load needs to be holding the cultural and collective dimensions, not just the individual presentation, or the work will reach a ceiling.

The same principle, in adapted form, applies for refugee-background clients, descendants of genocide survivors, and adults from families with persistent cycles of abuse. Treatment that ignores the wider load tends to underperform. Treatment that acknowledges and works with the load tends to produce more durable change.

For those who did not have the right buffering early, treatment genuinely helps

The single most important message from the treatment literature is that trauma is treatable. Adults who did not have adequate buffering in childhood are not stuck with the neurobiology that exposure produced. The brain retains plasticity throughout life, and structural and functional changes do reverse with effective treatment. Below is a summary of the interventions with the strongest evidence, drawn from the Australian Phoenix guidelines, the American Psychological Association guidelines, the United Kingdom National Institute for Health and Care Excellence guidelines, and the International Society for Traumatic Stress Studies guidelines, all of which converge on a similar set of first-line options.

First-line trauma-focused psychotherapies

Trauma-focused cognitive behavioural therapy is the most extensively evidence-based treatment for PTSD. The category includes cognitive processing therapy (CPT), prolonged exposure (PE), and trauma-focused cognitive therapy. These are recommended as first-line treatments in the Phoenix Australia, APA, NICE, and ISTSS guidelines (Phoenix Australia, 2020; American Psychological Association, 2017; NICE Guideline NG116, 2018; ISTSS, 2019). They work by helping the person process the traumatic memory, update the unhelpful beliefs the trauma created, and reduce the avoidance that maintains symptoms.

Eye movement desensitisation and reprocessing (EMDR), developed by Francine Shapiro, is also recommended as a first-line treatment in the major international guidelines. A meta-analysis of 26 randomised controlled trials published in PLOS One found significant reductions in PTSD symptoms (Hedges g = 0.66), depression, anxiety, and subjective distress (Chen et al., 2014). The mechanism is contested, with the Australian NHMRC guideline noting that treatment gains are more likely due to engagement with the traumatic memory and cognitive processing than to the eye movements themselves, but the clinical effect is well established.

Cognitive processing therapy and prolonged exposure are typically delivered in 8 to 16 sessions. EMDR is similarly time-limited. For people whose trauma is single-incident or relatively contained, these approaches frequently produce substantial symptom reduction within a few months.

For complex and developmental trauma

Adults who experienced sustained early-life adversity, prolonged interpersonal violence, or cumulative trauma across the lifespan often present with what is now classified in ICD-11 as complex PTSD. This includes the core PTSD symptoms plus pervasive emotional dysregulation, negative self-concept, and disturbances in relationships. The ISTSS expert consensus guidelines, with 84 per cent of expert clinicians endorsing the approach, recommend a phase-based or sequenced treatment (Cloitre et al., 2012). Phase one focuses on stabilisation, including emotion regulation skills, stress management, and safety. Phase two addresses trauma memory processing. Phase three focuses on reintegration, consolidating gains and rebuilding relationships, work, and community engagement.

The updated ISTSS guidance suggests that a more personalised approach may be appropriate rather than a strictly sequential application, since some people benefit from earlier memory processing while others need extended stabilisation first. This is another point where individual variation matters.

For emotional dysregulation

Dialectical behaviour therapy, developed by Marsha Linehan, has the strongest evidence base for the treatment of severe emotional dysregulation, particularly when it occurs in the context of borderline personality structure (Linehan, 1993; meta-analytic synthesis in multiple reviews). The four DBT skills modules (mindfulness, distress tolerance, emotion regulation, interpersonal effectiveness) address the specific deficits that follow developmental trauma. DBT was originally designed for chronically suicidal women with borderline personality disorder, a population previously considered untreatable. The treatment has since been adapted for adolescents, eating disorders, substance use, and PTSD with co-occurring emotion regulation difficulties.

Adjunctive and body-based approaches

Mindfulness-based stress reduction (MBSR) has accumulating evidence as an adjunctive intervention. A 2022 meta-analysis in Stress and Health found a moderate effect of MBSR on PTSD symptoms (Hedges g = 0.46) compared with treatment as usual (Liu et al., 2022). A subsequent 2024 systematic review of veteran populations found medium effects on both PTSD and depressive symptoms (Li et al., 2024). MBSR is not a substitute for trauma-focused therapy but is a useful complement, particularly for clients who need to build the regulatory capacity required to tolerate active trauma processing.

Yoga has been studied as an adjunctive intervention. Van der Kolk and colleagues (2014), in the Journal of Clinical Psychiatry, reported that trauma-sensitive yoga significantly reduced PTSD symptoms in chronically traumatised women, with effect sizes comparable to established psychotherapies. The mechanism is thought to involve interoceptive awareness, autonomic regulation, and rebuilding the relationship between body sensation and felt safety. For clients whose trauma is held strongly in somatic patterns, body-based approaches frequently add something that talking therapies on their own do not reach.

Physical activity has independent evidence for the prevention and treatment of depression and anxiety. A 2022 meta-analysis in JAMA Psychiatry, covering over two million person-years across 15 prospective studies, found that adults meeting standard physical activity recommendations (around 2.5 hours of brisk walking per week) had substantially lower risk of incident depression than physically inactive adults (Pearce et al., 2022). The dose-response curve is non-linear, with the largest gains at the bottom of the activity distribution, meaning that even modest movement matters for people who are currently sedentary.

Emerging treatments

MDMA-assisted psychotherapy has produced striking results in two phase 3 trials. Mitchell and colleagues (2021), publishing in Nature Medicine, reported that 67 per cent of participants who received MDMA-assisted therapy no longer met criteria for PTSD after three treatment sessions, compared with 32 per cent in the placebo-plus-therapy group. The 2023 follow-up phase 3 trial replicated the effect in a moderate-to-severe PTSD population (Mitchell et al., 2023). Regulatory pathways in Australia have moved ahead of most other jurisdictions, with the Therapeutic Goods Administration authorising MDMA for the treatment of PTSD under the Authorised Prescriber Scheme from July 2023. Access remains limited, and the treatment is not a stand-alone medication but a structured therapy with medicine-assisted sessions embedded in a longer protocol of preparation and integration.

Other emerging approaches with growing but earlier-stage evidence include ketamine for treatment-resistant depression and complex PTSD, transcranial magnetic stimulation, neurofeedback, and intensive group-based reintegration programs. These sit in the broader treatment landscape rather than as front-line recommendations.

What works varies by person, just like buffering does

The treatment guidelines converge on the major first-line options, but the within-person fit varies considerably. Some people thrive in structured cognitive processing therapy with weekly trauma worksheets. Others find that same approach overwhelming and do better with a slower, somatically-paced model. Some respond well to EMDR. Others find the bilateral stimulation more activating than helpful and need a different entry point. Some can benefit from group-based work. Others need the privacy of individual sessions. Neurodivergent adults often require adapted protocols that account for sensory sensitivities, executive functioning differences, and broader trauma definitions, since standard PTSD assessment tools were not designed with autistic or ADHD presentations in mind (Rumball, Happé & Grey, 2020).

The implication for someone who is considering treatment is that the first approach you try is not necessarily the approach you will end with. A good clinician matches the treatment to the person rather than the person to the treatment, and is willing to adjust when something is not working.

A final word

Modern adults are carrying more exposure than the equivalent cohorts of previous generations carried, and the neurobiological consequences are real. The population-level brain chemistry shift is reasonable to infer even where direct testing is not yet possible. None of this is permanent or deterministic. Buffering structures matter and can be built at any age. Treatment works, and the menu of evidence-based options is broader and more individualised than it has ever been. The path through is not a single one. It is a personal one, mapped carefully with someone who understands both the population-level evidence and the variation that makes you specifically yourself.

If this resonates

Behavioural Edge Psychology provides assessment and treatment for adults with trauma-related presentations, including complex PTSD, neurodivergent trauma profiles, and high-exposure professional groups. We use evidence-based, trauma-informed, neurodiversity-affirming approaches matched to the individual rather than to the diagnosis. Consulting rooms in Caulfield South and St Kilda, Victoria.

To book, visit behavioural-edge-psychology.au4.cliniko.com/bookings or contact the practice directly.

Frequently asked questions

These answers are written for adults seeking clear information about trauma and treatment. Each draws on the same evidence base referenced throughout this post.

What is intergenerational trauma?

Intergenerational trauma refers to the transmission of trauma effects from one generation to the next, even when the descendant has not directly experienced the original traumatic event. It transmits through four documented mechanisms, namely epigenetic changes (altered methylation of stress-regulation genes such as NR3C1 and FKBP5), in utero and perinatal effects on fetal stress system programming, attachment and parenting patterns, and ongoing social or structural conditions. The strongest human evidence supports parent-to-child effects, with grandparent-to-grandchild transmission documented but more contested (Yehuda et al., 2014, 2016, 2018; Bierer et al., 2020; Mulligan et al., 2025).

Are people today more traumatised than previous generations?

The evidence supports a yes with moderate to high confidence. Mean adverse childhood experience scores have risen from 0.79 for Americans born before 1940 to 2.74 for those born in 1998, with the 2018 birth cohort projected above 3 (Anderson et al., 2023). Indirect exposure through screens, news cycles, and live-streamed events has expanded dramatically. The neurobiological cascade that follows exposure is well documented. The clinical correlates, including rising rates of anxiety and depression in young adults and declining adolescent mental health metrics, are visible in epidemiological data across OECD countries.

What does trauma do to the brain?

Trauma exposure reliably affects three brain regions and several downstream systems. The hippocampus shows volume reduction and impaired neurogenesis. The amygdala shows increased reactivity and dendritic growth. The prefrontal cortex shows reduced volume and reduced top-down regulation. Connectivity between these regions is disrupted. Underneath these changes, the hypothalamic-pituitary-adrenal axis becomes dysregulated, brain-derived neurotrophic factor is suppressed, heart rate variability is reduced, and low-grade systemic inflammation is sustained. Epigenetic modifications to the glucocorticoid receptor gene have been documented in postmortem hippocampal tissue from individuals with histories of childhood abuse (Teicher et al., 2016; McEwen et al., 2016; McGowan et al., 2009).

What is the most effective treatment for PTSD?

The Phoenix Australia, American Psychological Association, NICE, and International Society for Traumatic Stress Studies guidelines converge on the same first-line treatments. These are trauma-focused cognitive behavioural therapy (including cognitive processing therapy and prolonged exposure) and eye movement desensitisation and reprocessing (EMDR). For PTSD that is single-incident or relatively contained, these approaches typically produce substantial symptom reduction within 8 to 16 sessions. The best fit varies by individual, since some clients do well with structured cognitive processing while others need a more somatically-paced approach.

What is complex PTSD and how is it different from PTSD?

Complex PTSD, classified in ICD-11, includes the three core PTSD symptom clusters (re-experiencing, avoidance, sense of current threat) plus three additional disturbances in self-organisation, namely pervasive emotional dysregulation, persistent negative self-concept, and disturbances in relationships. Complex PTSD usually follows sustained, repeated, or developmental trauma rather than a single incident. The ISTSS recommends phase-based treatment, with phase one focused on stabilisation, phase two on trauma memory processing, and phase three on reintegration (Cloitre et al., 2012). Treatment is typically longer than for standard PTSD.

Can trauma be inherited from your parents or grandparents?

Partly, yes. The evidence in humans is strongest for parent-to-child effects, where altered methylation of stress-regulation genes has been documented in adult offspring of Holocaust survivors (Yehuda et al., 2014, 2016; Bierer et al., 2020). The Mulligan et al. (2025) Syrian refugee study extended this to three generations, identifying differentially methylated regions associated with grandmother-line war exposure. The transgenerational claim beyond F2 remains contested in human research, and current structural conditions account for substantial variance in any case (Martin et al., 2025). Other transmission pathways, including in utero stress hormone exposure, attachment disruption, and ongoing social conditions, are well established.

Why do some people develop PTSD and others do not after the same event?

Individual susceptibility varies because of differences in pre-existing buffering structures, prior trauma history, neurobiological starting point, attachment history, genetic factors including FKBP5 variants, and social conditions during and after the event. The same exposure can produce sustained PTSD in one person and time-limited acute stress in another. Cohen and Wills (1985) demonstrated that social support buffers the impact of stressful life events on mental health outcomes, a finding supported by 23 subsequent meta-analyses covering more than 1.4 billion participants (Vila, 2021).

Can the brain recover from trauma?

Yes. The brain retains plasticity throughout life, and the structural and functional changes that follow trauma do reverse with effective treatment. Hippocampal volume increases have been documented after successful PTSD treatment. Amygdala reactivity reduces. Prefrontal regulation strengthens. Heart rate variability improves. The realistic timeline depends on the complexity and chronicity of the original trauma, the level of intergenerational load, and the fit between treatment and individual. Most adults seeking treatment for trauma-related conditions can expect meaningful improvement.

How does Aboriginal intergenerational trauma affect Australians today?

At least one-third of Aboriginal and Torres Strait Islander Australians are affected by intergenerational trauma as descendants of the Stolen Generations (AIHW, 2023). The trauma transmits through epigenetic changes, attachment disruption, ongoing structural racism, and cultural rupture (Atkinson, 2002). Mental disorders account for around 20 per cent of the Aboriginal and Torres Strait Islander health gap (Diminic et al., 2024). Healing is more effective when it is culturally grounded, community-held, and collective rather than delivered solely in individual therapy. Aboriginal community-controlled health services and trauma-informed culturally responsive frameworks are central to this work.

Where can I find a trauma psychologist in Melbourne?

Behavioural Edge Psychology provides assessment and treatment for adults with trauma-related presentations from consulting rooms in Caulfield South and St Kilda, Victoria. Dr Sarah Fischer is the Principal Psychologist, with AHPRA endorsement in organisational psychology, a PhD in psychology, and longstanding experience across clinical, medicolegal, WorkSafe Victoria, Transport Accident Commission, and NDIS contexts. Bookings can be made through the practice website. The Australian Psychological Society and Australian Clinical Psychology Association directories list additional trauma-focused psychologists across Victoria. Working with a psychologist who is registered with WorkSafe Victoria and the TAC may matter where the trauma is workplace or accident related.

References

• American Psychological Association. (2017). Clinical practice guideline for the treatment of posttraumatic stress disorder (PTSD) in adults. https://www.apa.org/ptsd-guideline

• Anderson, K. N., Swedo, E. A., Trinh, E., Ray, C. M., Krause, K. H., Verlenden, J. V., Clayton, H. B., Villaveces, A., Massetti, G. M., & Holditch Niolon, P. (2023). Trends and forecasted rates of adverse childhood experiences among adults in the United States. An analysis of the 2020 Behavioral Risk Factor Surveillance System.

• Atkinson, J. (2002). Trauma trails, recreating song lines. The transgenerational effects of trauma in Indigenous Australia. Spinifex Press.

• Australian Institute of Health and Welfare. (2023). Intergenerational trauma and mental health. Summary paper. https://www.aihw.gov.au/

• Benjet, C., Bromet, E., Karam, E. G., Kessler, R. C., McLaughlin, K. A., Ruscio, A. M., et al. (2016). The epidemiology of traumatic event exposure worldwide. Results from the World Mental Health Survey Consortium. Psychological Medicine, 46(2), 327 to 343.

• Bierer, L. M., Bader, H. N., Daskalakis, N. P., Lehrner, A., Provencal, N., Wiechmann, T., Klengel, T., Makotkine, I., Binder, E. B., & Yehuda, R. (2020). Intergenerational effects of maternal Holocaust exposure on FKBP5 methylation. American Journal of Psychiatry, 177(8), 744 to 753.

• Chen, Y. R., Hung, K. W., Tsai, J. C., Chu, H., Chung, M. H., Chen, S. R., Liao, Y. M., Ou, K. L., Chang, Y. C., & Chou, K. R. (2014). Efficacy of eye-movement desensitization and reprocessing for patients with posttraumatic-stress disorder. A meta-analysis of randomized controlled trials. PLOS ONE, 9(8), e103676.

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About the author

Dr Sarah Fischer is the Principal Psychologist of Behavioural Edge Psychology Pty Ltd, with consulting rooms in Caulfield South and St Kilda, Victoria. She holds a PhD in Psychology and a Master of Psychology and is AHPRA-endorsed in organisational psychology. She leads reflective practice and debriefing the Victorian legal sector to reduce impact of vicarious and direct trauma exposure at work. Her practice spans adult neurodivergence assessments using MIGDAS-2 and DIVA-5 protocols, clinical therapy for trauma and complex presentations, WorkSafe Victoria and Transport Accident Commission treating provider work, NDIS-registered services, and medicolegal independent medical examinations. Her therapeutic philosophy is trauma-informed, neurodiversity-affirming, and evidence-based.