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JMDk important definitions

 

What is "prolonged childhood adversity" mean?

What does "consciousness" mean?

What does "cognition" mean?

Prolonged childhood adversity

 

ISA's definition of "prolonged childhood adversity" is any repeated developmental trauma, especially associated with any of Bessel van der Kolk definitions of developmental trauma known as Complex Trauma [C-PTSD).

 

Emotional neglect

They also found that emotional neglect, among the trauma-related measures they tested, was the only one that showed a clear negative link with global hippocampal volume and several hippocampal subfields (Dimitrova, 2023).

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The current literature supports Integrative Self-Analysis’ core claim that "prolonged childhood adversity" can produce bottom-up biological changes across the following domains:

 

  • Epigenetic

  • Immune

  • Endocrine

  • Autonomic

  • Interoceptive Drive-States

 

Many of these changes do not require cognition (i.e. ego cognition, cognitive appraisal, self-awareness, apperception, explicit awareness, or interoception) to be initiated or maintained.

Jaguar Marigold ISA’s References

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Afrin, L. B., et al. (2017)

Alcaro and Carta (2019)

Alcaro and Panksepp (2014)

Arck, P. C., et al. (2006)

Bedard-Gilligan and Zoellner (2012)

Besedovsky et al. (1977)

Besedovsky and del Rey (2007)]

Bonaz, Sinniger, and Pellissier (2017)

Bonaz, Sinniger, and Pellissier (2018)

Bremner, J. D., et al. (1995)

Brewin (2018)

Dantzer, O’Connor, Freund, Johnson, and Kelley (2008)

Diano, Celeghin, Bagnis, and Tamietto (2017)

Dimitrova et al. (2023)

Chalavi et al. (2015)

Engel (1977)

Eisenberger, Berkman, Inagaki, Rameson, Mashal, and Irwin (2010)

Etkin, Egner, and Kalisch (2011)

Felger and Lotrich (2013)

Foster, Rinaman, and Cryan (2017)

Freeman and Elmadjian (1947)

Gorman, J. M., et al. (1984)

Harb, Liuzzi, Huggins, Webb, Fitzgerald, Krukowski, deRoon-Cassini, and Larson (2024)

Harper, R. M., et al. (2005)

Hosseini-Kamkar, et al. (2023)

Karimi, K., et al. (2000)

Kotulla, Elsenbruch, Roderigo, Brinkhoff, Wegner, Engler, Schedlowski, and Benson (2018)

Kumsta, Entringer, Hellhammer, and Wüst (2007)

Laffey and Kavanagh (2002)

Lanius et al. (2010)

Lanius, Frewen, Vermetten, and Yehuda (2015)

Lanius et al. (2002)

Lanius et al. (2018)

Lawrence and Scofield (2024)

Leech, Stapleton, and Patching (2024)

Leon, A., et al. (1994)

Liu and Gershon (2024)

Lyons-Ruth, Chasson, Khoury, and Ahtam (2024)

McEwen (1998)

McLaughlin, DeCross, Jovanovic, and Tottenham (2019)

Michopoulos, V., et al. (2017)

Miller (2025)

Miller and Raison (2016)

Miller, Chen, and Zhou (2007)

Miller and Cole (2012)

Nardi, A. E., et al. (2009)

Osimo, Baxter, Lewis, Jones, and Khandaker (2019)

Pariante and Lightman (2008)

Phillips and Elmadjian (1947)

Porges (2011)

Rauch, S. L., et al. (2006)

Ruge, Ehlers, Kastrinogiannis, Klingelhöfer-Jens, Koppold, Abend, and Lonsdorf (2024)

Sacu, et al. (2024)

Santamaría-García, Migeot, Medel, Hazelton, Teckentrup, Romero-Ortuno, Piguet, Lawor, Northoff, and Ibáñez (2025)

Savitz et al. (2004)

Shin and Liberzon (2010)

Smith, Xu, and Pollak (2025)

Solms (1997)

Solms (2015)

Solms (2021)

Solms (2026)

Solms and Panksepp (2012)

Sullivan and Opendak (2021)

Tan, et al. (2014)

Theoharides, T. C., et al. (2004)

Tracey (2009)

Turnbull & Solms (2002)

van der Kolk and Fisler (1995)

von Schröder et al. (2025)

Yehuda, R., et al. (1996)

Zagaria, Fiori, Vacca, Lombardo, Pariante, and Ballesio (2024)

Zhou and Ryan (2023)

Zierau, O., et al. (2012)

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Liu and Gershon (2024)

 

The Study

Liu and Gershon argue that the older endophenotype model in psychiatry was too narrow for current genetics and genomics research. An endophenotype is a measurable trait that sits between genes and a disorder, such as a brain signal, hormone pattern, cognitive style, or other body-based feature. The authors propose a broader definition, calling endophenotypes genetically influenced traits linked not only to illness itself, but also to related events like environmental risk, illness progression, treatment response, and resilience, and they replace the old rule of strict state-independence with a model that can include state-dependent traits, meaning traits that show up only at certain times or under certain conditions. They also add “genetic mediation,” meaning evidence that genetic influence helps connect the trait to the disorder, while warning that simple overlap is not enough because one gene can affect multiple traits without one directly causing the other. This matters because the paper is trying to improve how researchers connect genetic findings to actual biological and behavioral processes in psychiatric disorders.

 

ISA relevance

From an ISA view, the paper is consistent with the idea that important parts of later suffering may move through measurable body-and-brain pathways that are genetically influenced, developmentally timed, environmentally shaped, and sometimes only visible in certain states, rather than appearing first as cognition That fits an ISA reading in which a Malignant Complex could help organize stress-linked dysregulation across deeper biological layers while remaining partly outside egoic access, but this study does not directly test Malignant Complexes, dissociation, or any claim that such a pattern “epigenetically hijacks” genes. More cautiously, it supports the narrower point that psychiatric mechanisms may be harder to map because the pathways between genes, environment, intermediate traits, and illness are non-linear, state-dependent, and biologically distributed.

 

Reference

Liu, C., & Gershon, E. S. (2024). Endophenotype 2.0: Updated definitions and criteria for endophenotypes of psychiatric disorders, incorporating new technologies and findings. Translational Psychiatry, 14, Article 502. https://doi.org/10.1038/s41398-024-03195-1

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