The Psychoneurobiological Nexus of Dissociative Dependence

Integrated Causality of Addiction, Obesity, and Chronic Physical Illness

I. Introduction: Framing the Crisis in Integrated Health

The contemporary epidemiological landscape is marked by a synergistic increase in the prevalence of neurological, metabolic, and chronic inflammatory diseases. This rise runs parallel to growing clinical awareness regarding the pervasive exposure to psychological trauma and environmental stressors. This report establishes a unified theoretical model that links Adverse Childhood Experiences (ACEs) and the resultant trauma-related dissociation—specifically conceptualized through the framework of addiction provided by the Wounded Healers Institute (WHI) ¹—to the pathogenesis of obesity and systemic physical illness.

A. The Research Imperative: Moving Beyond Comorbidity to Integrated Causality

Traditional medical models often compartmentalize obesity, chronic pain, and inflammatory diseases as purely metabolic or lifestyle disorders, frequently failing to integrate the foundational role of psychological history in disease etiology. The goal of this analysis is to shift the conceptual framework from mere comorbidity, where conditions co-occur, toward a model of integrated causality, where one core psycho-biological mechanism drives both psychological and physical pathology. The failure to define addiction accurately in clinical and diagnostic frameworks ¹ has contributed significantly to this diagnostic segmentation, hindering effective treatment that addresses the root cause rather than symptomatic manifestations.

B. Overview of the Trauma-Dissociation-Metabolic Disease Axis

The central hypothesis posited herein is that chronic psychological trauma establishes a perpetual state of physiological dysregulation known as allostatic load.² This persistent stress state is subsequently managed through conditioned, trauma-informed dissociative and addictive coping mechanisms.¹ The adherence to these survival strategies directly drives the dysregulation of the neuroendocrine and immune systems, resulting in chronic systemic inflammation, profound metabolic dysfunction, and the eventual manifestation of obesity and widespread chronic physical illness.⁵

II. Psychological Precedent and Physiological Imprinting (The ACEs Foundation)

A. Adverse Childhood Experiences (ACEs): Quantitative Evidence of Dose-Dependent Risk

The pioneering ACE Study provided empirical validation that psychological stress is a critical predictor of later physical health. The seminal research, involving 17,000 adults, demonstrated a clear and strong correlation between the cumulative number of negative experiences during childhood (quantified as the ACE score) and a wide spectrum of poor health and behavioral outcomes in adult life.⁸

This correlation is characterized by a potent dose–response relationship: as the number of ACEs increases, the risk for developing chronic diseases, including ischemic heart disease, cancer, and chronic lung disease, rises significantly.⁸ The sheer predictive power of a psychological and social exposure (the ACE score) exceeding the predictive capacity of adult lifestyle factors alone underscores that trauma fundamentally alters homeostatic biology. This confirms that psychological stressors become biologically imprinted and are maintained as chronic physiological dysregulation, necessitating a profound shift in public health and clinical policy toward primary trauma prevention and trauma-informed care.

B. The Traumatogenic Cascade: Chronic Stress and Allostatic Load

The physiological consequence of chronic adversity is captured by the concept of allostatic load. Allostatic load is understood as the complex, non-linear “wear and tear” resulting from prolonged or poorly regulated adaptive efforts in response to repeated stress burdens.² This cumulative burden often synergizes with episodes of acute stress or trauma, establishing a chronic state of instability in the body.²

The prolonged and excessive production of stress hormones associated with allostatic load structurally compromises the body’s regulatory systems.³ This sustained instability increases susceptibility to a wide array of adverse health conditions, including cardiovascular disease, chronic pain, and posttraumatic stress disorder (PTSD).³ Research confirms that the chronic health sequelae associated with childhood abuse are overtly dose-dependent; the severity, frequency, and duration of the abuse are directly correlated with the extent of the resultant injury or illness experienced.³ This ongoing physiological stress acts as the primary mechanism translating psychological adversity (ACEs) into quantifiable, irreversible physical susceptibility. The body, therefore, maintains the “memory” of trauma not just as psychological material, but as measurable, persistent physiological stress markers, forming the foundation for all subsequent metabolic dysregulation.

C. Dissociation as a Biologically Necessary Survival Response

In the face of overwhelming or inescapable threat, the human psyche engages dissociation—a complex psychological process ranging from mild, everyday detachment (e.g., daydreaming) to severe identity fragmentation.¹ This mechanism is rooted in trauma and functions as a core survival strategy for managing affect that would otherwise overwhelm the system.⁴

The Wounded Healers Institute posits a specific framework for understanding addiction within this context. Addiction is defined as the pathological and conditioned relationship forged between unresolved trauma and the continued and unchecked progression of dissociative responses.¹ When trauma occurs, the organism utilizes endogenous systems, such as the opioid and cannabinoid pathways, for immediate survival and pain regulation.¹ The overwhelming nature of the traumatic experience causes the body to bond—an implicit process akin to trauma-bonding or conditioning—to the resulting state of chemical dissociation (numbness or instantaneous relief). This bond, rather than the substance or behavior itself, becomes the defining addictive mechanism.¹ Consequently, the compulsive or addictive drive is functionally an instinctual imperative toward this pathologically conditioned survival state. The system requires the dissociative state to regulate, regardless of the destructive long-term costs.

III. The Addictive Mechanism of Trauma-Related Dissociation

A. Phenomenology of Active Addiction: Loss of Control as Survival Override

The subjective experience of active addiction, as captured through phenomenological inquiry, reveals a state of profound psychological bondage. Participants consistently describe feeling “trapped,” “enslaved,” “owned,” or living in an “out of control” state where the core, conscious self is fundamentally sidelined.¹ Expressions of being “driven” or controlled by an internal “creature” ¹ represent the psychological consequence of the brain being hijacked by an Emotional Part (EP) or primal action system designed for immediate threat response.

The WHI conceptualizes this phenomenon through the thesis that addictions constitute a conditioned bond to a dissociative state, the primary purpose of which is to ensure survival and regulation by any means necessary.¹ The perception of being “out of control” arises when the primitive, unconscious brain (the reptilian/EP systems) takes command. This primitive system acts according to an unconscious mandate of immediate preservation, prioritizing short-term regulation over the long-term consequences calculated by the cognitive brain (the Appearing Normal Part, ANP).¹ This explanatory framework effectively resolves the perennial “choice vs. disease” debate in addictionology: the disease is understood as the lack of conscious regulatory choice, and the addictive act is functionally an unconscious, survival choice executed under chronic physiological duress.

B. Neurobiological Basis of the Dissociative Bond

The neurological commonality between psychological trauma and addiction is extensive. Withdrawal symptoms, for instance, are observed to mimic the clinical symptoms of PTSD neurologically, confirming that both trauma adaptation and chemical dependency involve the same foundational endogenous opiate system.¹ Further supporting this shared etiology, the opiate antagonist Naltrexone is clinically effective in treating both conventional addiction (e.g., alcohol, cocaine, gambling) and pathological clinical dissociation.¹ This pharmacological overlap provides direct evidence that both conditions rely upon the same foundational regulatory pathway for managing profound distress.

In this model, traditionally defined addiction symptoms acquire new clinical meaning. Cravings, urges, and the increase in time spent preoccupied with obtaining the substance or engaging in the behavior are more accurately characterized as intrusive reminders or somatic flashbacks—unconscious material demanding immediate homeostatic regulation.¹ The compulsion to use is driven by the traumatic memory demanding discharge or replication. Because addiction memory is biologically akin to traumatic memory, treatment success mandates strategies focused on memory reconsolidation (trauma resolution), rather than solely behavioral modification.¹ Failure to address the core addiction memory network ensures the persistent drive toward dissociative reenactment, fueling cravings, compulsion, and the high propensity for addiction transferability.

IV. Compulsive Consumption, Obesity, and Metabolic Overlap

A. Obesity as a Trauma-Related Condition: Epidemiological and Developmental Links

Epidemiological evidence establishes a significant association between ACEs and the risk of developing childhood obesity.¹⁰ Specific forms of abuse, such as sexual abuse, appear to have a particularly pronounced effect on elevating childhood obesity risk compared to other categories of ACEs.¹⁰

A critical finding concerns the temporal course of this link: the effect of ACEs on the development of childhood obesity often exhibits a substantial latency, taking approximately two to five years to manifest clinically.¹⁰ This delay indicates that the link is not merely a transient consequence of immediate behavioral change (e.g., stress eating in the moment), but rather a profound and sustained metabolic reprogramming orchestrated by chronic stress. The sustained allostatic load established by the trauma history ² forces a fundamental shift in the body’s metabolic set point, leading to chronic dysregulation of fat storage hormones, appetite regulation, and inflammation—the biological precursors of Metabolic Syndrome—which only emerge clinically years after the initial trauma exposure. Obesity, therefore, functions as a delayed somatic expression of allostatic failure.

B. Neurobiological Equivalence of Binge Eating and Addiction (BED/SUDs)

The neurobiological overlap between Binge Eating Disorder (BED) and substance use addictions (SUDs) is substantial, characterized by mirroring symptomatic presentations. Both conditions demonstrate increased tolerance to the amount consumed, intense triggering urges, and shared activity across the dopaminergic and opiate reward pathways.⁹

Crucially, dissociation serves as a primary coping mechanism within eating disorders for managing intense, overwhelming emotions arising from both traumatic and non-traumatic events.⁴ Given that consumption of highly palatable, hyper-processed food strongly activates the same opioid and dopamine reward pathways as illicit substances ⁹, food functions as an easily accessible, immediate chemical dissociative agent. Compulsive consumption (bingeing) is understood as the behavioral reenactment designed to induce the necessary dissociative state for emotional regulation and profound numbing.¹ In this context, obesity is the physical, dose-dependent consequence of an untreated emotional regulation failure rooted in chronic trauma.

Table 2: Unified Model of Compulsive Consumption: Overlap of Mechanisms

Pathology Domain	SUD/Addiction (WHI Framework)	Binge Eating Disorder (BED)	Trauma-Related Dissociation (Pathogenic Role)
Core Phenomenological State	Compulsion, Loss of Control, Feeling “Owned” or “Enslaved” 1	Bingeing, Hyperphagia, Emotional Eating	Somatic/Emotional Fragmentation, Amnesia, Overridden Consciousness 1
Neurobiological Substrate	Dopamine/Reward Dysfunction; Opioid Signaling (Endogenous Systems)	Shared Dopaminergic and Opiate Pathways 9; Cannabinoid Involvement	Endogenous Opioid/Cannabinoid Release (Numbing/Relief) 1
Primary Function (Survival Agenda)	Conditioned bond to the dissociative state to regulate overwhelming stress/pain (Relief Seeking) 1	Avoidance of intense/negative affect; Emotional Regulation mechanism 4	Survival/Regulation in the face of perceived life threat; Instinctual pursuit of homeostasis (The ‘Greater Good’) 1

C. Serotonin Pathways, Metabolic Regulation, and Dysfunction

The monoamine serotonin (5-hydroxytryptamine, 5-HT) is central to both psychological and physiological regulation, modulating mood and feeding behaviors within the central nervous system.¹¹ Disruption of the peripheral serotonergic system and its receptors is closely associated with obesity and diabetes.¹¹ Peripheral 5-HT plays a vital role in general metabolic regulation, specifically suppressing adaptive thermogenesis in brown adipose tissue. Experimental inhibition of peripheral 5-HT synthesis has been demonstrated to reduce weight gain and improve metabolic dysfunction in diet-induced obesity mouse models.¹¹

The 5-HT2A receptor acts as a shared pathological pathway, linking both cognitive functions (implicated in schizophrenia and affective disorders) and peripheral cardiovascular function (vasoconstriction, hypertension).¹² This link explains the high rates of metabolic comorbidity: Metabolic syndrome is reported in approximately 40% of schizophrenic patients and 25% of patients with recurrent depression.¹² The existence of this dual functionality confirms that chronic psychological stress and resultant neuroendocrine dysfunction (dissociation/addiction) inherently involve systemic metabolic disruption. Metabolic illness, therefore, can be viewed as a chronic physical manifestation of dysregulated 5-HT, driven by sustained trauma and allostatic load.

V. Biological Mechanisms and Systemic Inflammation

A. The Trauma-Immune Connection: Dissociation and Accelerated Aging

The cumulative impact of chronic trauma on systemic health is starkly visible in the immune system. Individuals, such as Veterans with PTSD, exhibit a high burden of diseases typically associated with accelerated aging, including cardiovascular disease, autoimmune disorders, and dementia.⁵ PTSD is consistently linked to a chronic pro-inflammatory activation of the immune system, characterized by sustained elevations in pro-inflammatory cytokines, specifically interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and interferon $\gamma$ (IFN gamma).⁵ This chronic inflammatory state functions as the primary physiological engine driving “accelerated aging” and the early onset of age-related physical diseases in trauma-exposed populations.⁵ This prolonged state of immune mobilization is the necessary biological precursor for chronic metabolic and neurological dysfunction.

B. Dissociation as an Active Inflammatory Mediator

The relationship between trauma, dissociation, and inflammation is intimate. General dissociation, a mechanism of managing trauma exposure, is statistically associated with higher concentrations of C-Reactive Protein (CRP)—a key marker of systemic inflammation—among traumatized women with Type 2 Diabetes Mellitus (T2DM).⁶ Critically, this association is independent of the severity of trauma exposure or the presence of a current psychiatric diagnosis.⁶

This finding establishes dissociation itself as an active pathogenic factor, not merely a passive symptom of trauma. The physiological act of maintaining the psychological split (structural dissociation) demands a high, chronic state of immune activation, as the body is perpetually defending itself against an internal enemy: the perceived threat posed by the unprocessed, somatically stored trauma.¹ This pathological state drives systemic inflammation (high CRP) ⁶, which, in turn, fuels insulin resistance, T2DM, and obesity. The resulting physical deterioration further exacerbates psychological distress, locking the system into a perpetual trauma-dissociation-inflammation cycle. Resolving dissociation is thus physiologically required to subdue the chronic inflammatory state and mitigate disease progression.

C. Metabolic Consequences of Chronic Dissociative Stress

The systemic inflammation generated by sustained allostatic load and active dissociation directly compromises metabolic health. This chronic inflammation reduces the efficacy of insulin receptors and promotes the synthesis of reactive oxygen species (ROS), H2H2 leading to oxidative damage.⁷ Furthermore, it increases the production of potent pro-inflammatory factors, including JNK IKK beta, and NF\kappa\B.⁷ These processes directly lead to insulin resistance, widespread glucose metabolism impairment, and excessive fat accumulation, culminating in the manifestation of Metabolic Syndrome and obesity.⁷ The body, perpetually primed in survival mode by dissociation, prioritizes emergency energy retention and sustained inflammation over balanced metabolic homeostasis.

Table 3: Biological Markers of Trauma-Related Allostatic Load and Metabolic Risk

System	Indicator/Marker	Relevance to Trauma/Dissociation	Mechanistic Pathway Link	Link to Metabolic Dysfunction/Obesity
Immune/Inflammation	C-Reactive Protein (CRP), IL-6, TNF-$\alpha$	Elevated in chronic PTSD and general dissociation 5	Active mechanism driving systemic wear-and-tear; Chronic immune defense 6	Predictor of cardiovascular disease and insulin resistance
Endocrine/Neuroendocrine	Melatonin/Serotonin Synthesis	Disrupted due to glyphosate/aluminum induced pineal gland pathology 1	Compromised sleep/restorative function; Imbalanced feeding/mood regulation 11	Sleep disorders, mood disorders, linked to obesity and diabetes pathways 11
Metabolic Stress	Anemia/Hypoxia (Iron/Cobalt deficiency)	Induced by synergistic exposure to Glyphosate and Aluminum 1	Promotes neurotoxicity and enhances aluminum uptake in brain; Impairs heme/CYP function 1	Chronic physiological stress driving energy retention and metabolic breakdown
Metabolic Drivers	JNK, IKK beta, and NF\kappa\B (Pro-inflammatory factors)	Increased production in response to environmental toxins (e.g., Glyphosate) 7	Directly drives insulin receptor impairment and tissue damage	Drives insulin resistance and fat accumulation (obesogenic effect) 7

VI. Environmental and Toxicological Synergies

A. Glyphosate, Aluminum, and Neurotoxicity: Mimicking Trauma States

Environmental toxicants exert a profound and synergistic pressure on the same biological systems compromised by psychological trauma. Epidemiological data demonstrate a remarkably strong correlation between the dramatic increase in glyphosate application on corn and soy crops in the United States and the rising prevalence of multiple neurological disorders, including autism, ADHD, anxiety disorder, and dementia.⁸

Aluminum and glyphosate are shown to synergistically induce neurological damage, leading specifically to pineal gland pathology and subsequent abnormal sleep patterns.¹ The pineal gland is highly susceptible to toxicant accumulation, accumulating aluminum at a rate at least twice that of other brain regions.¹ The symptoms induced by this toxic exposure—including sleep disturbance, anxiety, and dementia ¹—are clinically identical to those caused by psychological trauma. This confluence confirms the existence of a shared final common pathway for systemic stress: whether the stressor originates from a childhood ACE or chronic toxic exposure, the physiological outcome involves allostatic load, neuroendocrine dysfunction (pineal gland damage), and sustained systemic inflammation.⁵

B. Impaired Tryptophan Metabolism and Serotonin/Melatonin Disruption

Glyphosate, the active ingredient in Roundup, disrupts gut bacteria, favoring the overgrowth of pathogens such as Clostridium difficile, which produces the toxic metabolite p-cresol.¹ Furthermore, glyphosate actively blocks the shikimate pathway in plants and gut microbes, which are essential for synthesizing aromatic amino acids, including tryptophan—the sole precursor for both serotonin and melatonin.¹

Both glyphosate and aluminum further disrupt detoxification processes by interfering with Cytochrome P450 (CYP) enzymes, which are necessary for melatonin sulfation and metabolism.¹ This chemical disruption of fundamental neurochemical synthesis impairs the body’s ability to produce essential regulatory hormones. The resulting deficiency in serotonin and melatonin leads directly to pineal gland dysfunction and sleep disorders.¹ Impaired sleep further inhibits the brain’s glymphatic system, which is responsible for clearing cellular debris (the restorative function of sleep) ¹, thereby accelerating neurological and metabolic damage. This systemic sabotage by environmental toxins creates a deep physiological vulnerability, stripping the individual of the biological resources necessary to cope with psychological trauma and locking the trauma survivor deeper into the addictive/dissociative state.

C. The Hypoxia-Anemia-Aluminum Pathway and Metabolic Damage

The synergy between glyphosate and aluminum generates a cascade of physiological stress. Both toxicants induce anemia, which results in hypoxia (insufficient oxygen-carrying capacity).¹ Hypoxia, in turn, triggers increased synthesis of transferrin in the pineal gland, which enhances aluminum uptake into brain tissue (an uptake process further amplified by p-cresol, a glyphosate-induced toxic gut metabolite).¹

This toxicological stress cascade (toxin rightarrow anemia rightarrow hypoxia) is a profound metabolic stressor. Moreover, glyphosate is recognized as a strong human endocrine disruptor, directly linked to elevations in glucose and insulin levels, adverse fat distribution (obesity), and is strongly associated with the induction of insulin resistance and the full Metabolic Syndrome profile.⁷ Exposure to other common pesticides also demonstrates synergistic obesogenic effects.¹³ This establishes that environmental toxicity actively contributes to the obesity epidemic by exacerbating the metabolic damage initially caused by ACEs and allostatic load, driving the body toward a state of systemic metabolic failure and energy retention.

VII. Integrated Analysis and Clinical Implications

A. Synthesis: The Addictive Stress Cascade

The analysis confirms a unified, cyclical etiology for chronic disease, rooted in psychological trauma and mediated by pathological addiction (dissociation). Chronic psychological trauma initiates a sustained survival response (allostatic load) ³, which is managed through the pathological bond to dissociation (Addiction).¹ This addictive dissociation maintains chronic systemic inflammation ⁶, which, when compounded by environmental neurotoxicity (glyphosate and aluminum disrupting pineal and metabolic pathways) ¹, fundamentally dysregulates metabolic and neuroendocrine systems, leading to obesity and chronic physical disease.⁷

The compulsion experienced by the trauma survivor is the psychological manifestation—a conditioned pursuit of safety or relief via the dissociative split (EP systems dominating the ANP).¹ The resulting obesity and Type 2 Diabetes are the metabolic manifestations—the physical consequences of the body being locked into a chronic, energy-retentive survival state due to stress and toxicological damage.⁷

B. Clinical Implications for Trauma-Informed Treatment of Obesity and Chronic Illness

Recognizing that obesity, chronic inflammation, and cardiovascular risk are trauma-driven pathologies has profound clinical implications. Treating these conditions without resolving the underlying ACEs and the resulting addictive/dissociative coping mechanisms will predictably lead to repeated therapeutic failure, as the biological imperative to seek safety via dissociation remains fundamentally unchecked.

Therapeutic interventions must shift focus to directly address the core traumatic memory and the conditioned dissociative response.¹ Techniques that specifically promote memory reconsolidation (e.g., Eye Movement Desensitization and Reprocessing ¹, somatic experiencing) are critical for dismantling the deeply encoded “addiction memory” and neutralizing the relentless, intrusive compulsive drive.¹ Furthermore, compulsive consumption, such as binge eating, must be understood as a profound failure of affective regulation and a dissociative reenactment ⁴, requiring treatment that moves beyond punitive caloric restriction to manage the underlying emotional triggers.

C. The Role of Memory Reconsolidation in Physiological Regulation

The WHI model establishes that addiction is the bond to the unresolved trauma or dissociative response.¹ Therefore, successful, long-term recovery depends entirely on resolving that memory. Memory reconsolidation processes neutralize the emotional charge and implicit fear associated with the traumatic or addictive memory, thereby eliminating the instinctive, relentless drive for the dissociative reenactment (compulsion/craving).¹ This psychological restructuring leads directly to long-term neurobiological and metabolic stability by suppressing the chronic stress and inflammatory cycle driven by the unresolved trauma.

VIII. Conclusions and Recommendations

The exhaustive analysis presented here demonstrates that the epidemics of obesity, neurological disorders, and chronic inflammatory diseases are inextricably linked by a shared psychoneurobiological pathway initiated by chronic psychological trauma (ACEs). The resulting allostatic load is managed through the pathological, conditioned pursuit of dissociation, a mechanism that perfectly aligns with clinical definitions of addiction. This addictive dissociation actively drives systemic inflammation and metabolic failure.

A. Recommendations for Clinical Practice

1. Offer Trauma-Focused Treatment for Metabolic Disorders: Clinicians treating obesity, Type 2 Diabetes, and cardiovascular disease must screen for ACEs and incorporate trauma-resolution therapies, such as EMDR, as a standard component of care. Treating physical pathology without addressing the underlying addiction memory and dissociative survival mechanism will perpetuate the cycle of chronic illness and relapse.¹
2. Redefine Compulsive Consumption: Compulsive eating and binge eating must be clinically classified as manifestations of trauma-related dissociation, requiring specialized treatment aimed at emotional regulation and memory reconsolidation rather than punitive behavioral modification.⁴
3. Acknowledge Dissociation as a Pathogenic Factor: Clinicians must recognize that the psychological maintenance of dissociation itself drives systemic inflammation (high CRP).⁶ Therapeutic success requires actively addressing the dissociative splitting mechanism to quiet the body’s chronic defense response.

B. Recommendations for Public Health and Policy

1. Universal ACEs Screening and Prevention: Implement mandatory, universal ACEs screening in all primary and pediatric care settings to quantify individual risk and deploy early intervention strategies before metabolic consequences manifest years later.⁸
2. Integrated Care Systems: Policy must mandate the creation of integrated physical and behavioral health care models that treat systemic inflammation, obesity, and cardiovascular risk as trauma-driven pathology, thereby dismantling the traditional siloed approach to mind and body illness.
3. Environmental Toxicant Regulation: Aggressively regulate environmental chemicals, particularly glyphosate and aluminum, due to their documented synergistic neurotoxic effects. These toxins compound psychological trauma by damaging the neuroendocrine system (pineal gland, melatonin/serotonin synthesis) and directly driving insulin resistance, thereby accelerating the metabolic disease trajectory in the stress-primed population.⁷

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References

O’Brien, A. (2023a). Addiction as Trauma-Related Dissociation: A Phenomenological Investigation of the Addictive State. International University of Graduate Studies. (Dissertation). Retrieved at woundedhealersinstitute.org/courses/addiction-as-dissociation-model-course/

O’Brien, A. (2023b). Memory Reconsolidation in Psychedelics Therapy. In Path of the Wounded Healer: A Dissociative-Focused Phase Model for Normative and Pathological States of Consciousness: Training Manual and Guide. Albany, NY: Wounded Healers Institute. Retrieved at woundedhealersinstitute.org/courses/addiction-as-dissociation-model-course/

O’Brien, A. (2023c). Path of the Wounded Healer: A Dissociative-Focused Phase Model for Normative and Pathological States of Consciousness: Training Manual and Guide. Albany, NY: Wounded Healers Institute. Retrieved at woundedhealersinstitute.org/

O’Brien, A. (2024a). Healer and Healing: The re-education of the healer and healing professions as an advocation. Re-educational and Training Manual and Guide. Albany, NY: Wounded Healers Institute. Retrieved at woundedhealersinstitute.org/

O’Brien, A. (2024e). Path of the Wounded Healers for Thrivers: Perfectionism, Altruism, and Ambition Addictions; Re-education and training manual for Abusers, Activists, Batterers, Bullies, Enablers, Killers, Narcissists, Offenders, Parents, Perpetrators, and Warriors. Re-Education and Training Manual and Guide. Albany, NY: Wounded Healers Institute. Retrieved at woundedhealersinstitute.org/

O’Brien, A. (2025). American Made Addiction Recovery: a healer’s journey through professional recovery. Albany, NY: Wounded Healers Institute. Retrieved at woundedhealersinstitute.org/

*This is for informational and educational purposes only. For medical advice or diagnosis, consult a professional.