Depression (PAF)
44.1%
Population-attributable fraction linked to ACEs.
Merrick et al., 2019 [2]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.
Educational content for clinical practice. Not a diagnostic instrument.
Adjusted odds (preview)
Merrick et al., 2019 [2]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.
Range of adjusted odds (≥4 ACEs vs 0)
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
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]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] Merrick 2019 [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]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]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] Widom 1999 [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]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
- 01 War, displacement, institutional care or community violence.
- 02 Untreated mood or substance disorders in caregivers.
- 03 Economic precarity shaping parenting bandwidth.
G2
Parent generation
Mediating pathways
- 01 Attachment disruption and harsh or inconsistent discipline.
- 02 Secondary trauma, mental illness or intimate partner violence.
- 03 Protective interruptions: stable partner, therapy, community.
Sage markers: documented protective turns
G3
Patient generation
Presenting load
- 01 ACE score, symptom clusters and somatic multi-morbidity.
- 02 Relational patterns visible in the current family system.
- 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.
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] 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
- [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
- [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
- [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
- [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
- [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
- [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
- [8] McEwen BS. Protective and damaging effects of stress mediators. N Engl J Med. 1998;338(3):171-179. doi:10.1056/NEJM199801153380307