Clinician brief # Adversity has a measurable physiology, and it can be mapped across generations. Peer-reviewed findings, cited inline, built into a collaborative clinical tool. [Open traumaroots](https://app.traumaroots.com) [See the evidence](#evidence) Educational content for clinical practice. Not a diagnostic instrument. ## Adjusted odds (preview) Merrick et al., 2019 [[2]](#ref-2) Depression 5.3× COPD 2.8× Coronary heart disease 1.8× Heavy drinking 1.8× Adjusted odds ratios for four or more ACE categories compared with none, from a 25-state US survey (Merrick 2019). Population averages, not a prediction for one person. Evidence base ## What the data shows Population studies link cumulative adverse childhood experiences (ACEs) to adult disease burden in a graded, dose-response pattern. Figures below are adjusted odds ranges or population-attributable fractions from the cited sources. ### Adjusted odds by outcome Felitti 1998: four or more categories of childhood exposure compared with none. Felitti et al., 1998 [[1]](#ref-1) Range of adjusted odds (≥4 ACEs vs 0) Alcoholism, drug abuse, depression, suicide attempt 4-12× Smoking, poor self-rated health 2-4× Physical inactivity, severe obesity 1.4-1.6× Bars run to the top of each range reported in the original ACE Study (Felitti 1998). The label gives the full range. Population averages, not a prediction for one person. #### Protective and resilience factors Safe, stable caregiving, later therapeutic alliance and socioeconomic buffers attenuate risk trajectories. Map both risk exposures and protective relationships when constructing the genogram. Series colour: sage = protective / resilience context Risk elevation Protective Depression (PAF) 44.1% Population-attributable fraction linked to ACEs. Merrick et al., 2019 [[2]](#ref-2) COPD (PAF) 27.0% Population-attributable fraction linked to ACEs. Merrick et al., 2019 [[2]](#ref-2) Heavy drinking (PAF) 23.9% Population-attributable fraction linked to ACEs. Merrick et al., 2019 [[2]](#ref-2) Suicide attempts (range) 67-80% Estimated attributable fraction across ACE exposure. Dube et al., 2001 [[3]](#ref-3) Organ systems ## Physical and mental effects Adversity is not only a psychiatric history item. It associates with multi-system dysregulation: cardiovascular, respiratory, immune, metabolic and neuropsychiatric pathways. ### Cardiovascular Elevated odds of ischemic heart disease and related risk with higher ACE scores. Chronic stress physiology and behavioural pathways both implicated. Felitti et al., 1998 [[1]](#ref-1) ### Respiratory Graded association with chronic obstructive pulmonary disease and related lung disease. Smoking initiation and persistence partially mediate, residual risk remains. Felitti et al., 1998 [[1]](#ref-1)· Merrick 2019 [[2]](#ref-2) ### Immune Hospitalised autoimmune disease risk elevated approximately 70 to 100 percent with childhood adversity markers. Inflammatory set-points shift under chronic stress. +70-100% autoimmune hospitalisation Dube et al., 2009 [[4]](#ref-4) ### Metabolic and inflammation Childhood maltreatment associates with elevated C-reactive protein in adulthood (relative risk 2.07 in a prospective birth-cohort study), a marker of low-grade systemic inflammation. RR 2.07 CRP elevation Danese et al., 2008 [[5]](#ref-5) ### Neuropsychiatric Structural and functional brain differences documented after severe childhood maltreatment (hippocampus, amygdala, prefrontal networks). PTSD risk markedly elevated after childhood victimisation. Teicher & Samson, 2013 [[6]](#ref-6)· Widom 1999 [[7]](#ref-7) ### Allostatic load Cumulative wear from repeated stress-system activation (HPA axis, autonomic, metabolic). A useful framing for multi-morbidity without reducing the patient to a single diagnosis. McEwen 1998 [[8]](#ref-8) Transmission ## It did not start with the patient Intergenerational patterns are clinically observable. Mechanisms (behavioural modelling, attachment, socioeconomic continuity, possible epigenetic marks) remain an active research area. Treat early findings as hypothesis-generating, not settled law. Small early studies; not settled. Use as clinical context, not deterministic prediction. G1 ### Grandparent generation Historical exposures 1. 01 War, displacement, institutional care or community violence. 2. 02 Untreated mood or substance disorders in caregivers. 3. 03 Economic precarity shaping parenting bandwidth. G2 ### Parent generation Mediating pathways 1. 01 Attachment disruption and harsh or inconsistent discipline. 2. 02 Secondary trauma, mental illness or intimate partner violence. 3. 03 Protective interruptions: stable partner, therapy, community. Sage markers: documented protective turns G3 ### Patient generation Presenting load 1. 01 ACE score, symptom clusters and somatic multi-morbidity. 2. 02 Relational patterns visible in the current family system. 3. 03 Agency: documentation, treatment and deliberate repair. Clinical use: construct a three-generation genogram with medical, emotional and abuse-link notation. Record uncertainty explicitly. Do not overstate epigenetic claims in notes or reports. Application ## From data to the family room traumaroots is a collaborative genogram and casefile environment. It turns population evidence into a shared, editable map you can use with patients, families and the treating team in real time.  Physical symptoms across generations, visible at a glance. ### Multi-user real-time sessions Clinician, therapist and consenting family members can view and edit the same tree concurrently. Presence indicators and conflict-safe updates keep the session coherent. ### Casefiles Structured case containers for longitudinal work: session notes linkage, export for records and controlled sharing without scattering diagrams across personal drives. ### Clinical notation layers Medical, emotional and abuse-link facets can be toggled independently. Notation stays on the diagram where pattern recognition happens, not buried in free text alone. ### Patterns across generations Visual continuity of illness, caregiving, rupture and repair. Supports formulation discussions and discharge planning with a shared reference object. [Open traumaroots](https://app.traumaroots.com) [App features](https://traumaroots.com/features) Roadmap - Pattern insights - Guided timeline views [What's next](https://traumaroots.com/coming-soon) Questions ## FAQ ### Is traumaroots a diagnostic tool? No. It supports documentation, formulation and collaborative mapping. Clinical judgment and validated instruments remain the responsibility of the treating clinician. ### How are citations handled on this page? Every quantitative claim carries a numbered reference. Full citations appear in the References section below. Prefer primary sources when citing in your own work. ### Can I work live with a therapist and patient? Yes. Multi-user sessions are a core differentiator. Access is consent-gated and role-aware. ### Where is the product based? Australia first (traumaroots.com and whathappenedto.me). Crisis numbers on this page are Australian services. ## References Numbered citations as used above. Links go to publisher or DOI pages where available. Verify against the primary literature before clinical or academic reuse. 1. [1] Felitti VJ, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults: The Adverse Childhood Experiences (ACE) Study. Am J Prev Med. 1998;14(4):245-258. [doi:10.1016/S0749-3797(98)00017-8](https://doi.org/10.1016/S0749-3797(98)00017-8) 2. [2] Merrick MT, et al. Vital Signs: Estimated Proportion of Adult Health Problems Attributable to Adverse Childhood Experiences and Implications for Prevention, 25 States, 2015-2017. MMWR. 2019;68(44):999-1005. [doi:10.15585/mmwr.mm6844e1](https://doi.org/10.15585/mmwr.mm6844e1) 3. [3] Dube SR, et al. Childhood abuse, household dysfunction, and the risk of attempted suicide throughout the life span: findings from the ACE Study. JAMA. 2001;286(24):3089-3096. [doi:10.1001/jama.286.24.3089](https://doi.org/10.1001/jama.286.24.3089) 4. [4] Dube SR, et al. Cumulative childhood stress and autoimmune diseases in adults. Psychosom Med. 2009;71(2):243-250. [doi:10.1097/PSY.0b013e3181907888](https://doi.org/10.1097/PSY.0b013e3181907888) 5. [5] Danese A, et al. Elevated inflammation levels in depressed adults with a history of childhood maltreatment (relative risk 2.07). Arch Gen Psychiatry. 2008;65(4):409-415. [doi:10.1001/archpsyc.65.4.409](https://doi.org/10.1001/archpsyc.65.4.409) 6. [6] Teicher MH, Samson JA. Childhood maltreatment and psychopathology: A case for ecophenotypic variants as clinically and neurobiologically distinct subtypes. See also Teicher and Samson, 2016 annual review on neurobiological consequences. Am J Psychiatry. 2013;170(10):1114-1133. [doi:10.1176/appi.ajp.2013.12070957](https://doi.org/10.1176/appi.ajp.2013.12070957) 7. [7] Widom CS. Posttraumatic stress disorder in abused and neglected children grown up. Am J Psychiatry. 1999;156(8):1223-1229. [doi:10.1176/ajp.156.8.1223](https://doi.org/10.1176/ajp.156.8.1223) 8. [8] McEwen BS. Protective and damaging effects of stress mediators. N Engl J Med. 1998;338(3):171-179. [doi:10.1056/NEJM199801153380307](https://doi.org/10.1056/NEJM199801153380307) --- Canonical page: