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Chapter 12.  Mental Health

Neuropsychiatric Instability as a Consequence of Toxicant and Traumatic Exposure. Reframing the Narrative:

From Stigma to Structural Injury

​ ~ We don’t need to reinvent psychiatry. We must realign it with biology, integrating trauma-informed care with a parallel commitment to exposure-aware diagnostics and treatment that acknowledges the impact of toxic exposures.

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This chapter confronts the persistent misclassification of mental health symptoms among chemically exposed veterans, particularly those with comorbid mild traumatic brain injury (mTBI). It reframes emotional and cognitive dysregulation not as psychiatric disease in isolation, but as the downstream result of measurable molecular and structural injury to brain systems governing affect, memory, and resilience.

 

BioSymphony models the lived experience of one such survivor. Diagnosed with various chemically induced conditions over time - including ADHD, treatment-resistant depression, and exacerbated PTSD  - his clinical history mirrors that of many veterans: a life reshaped not by trauma alone, but by unrecognized neural, microvascular, genomic damage, and epigenetic remodeling of tissue, stemming from sustained dermal exposure to permethrin and DEET, compounded by field-acquired mTBI.

 

The evidence does not negate emotional suffering - it reclassifies it. What has been labeled as emotional instability is, in fact, limbic microglial activation. What has been called anxiety is baroreflex failure and vagal hypersensitivity. What’s dismissed as depression is often NAD⁺ depletion and prefrontal synaptic collapse.

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A Common Pattern, Too Often Missed

 

 

The survivor is not alone. The chapter’s findings also speak to the many we have lost - veterans who died by suicide after exhibiting similar symptom profiles: profound fatigue, cognitive fragmentation, emotional volatility, and episodes of intense fear or dissociation without clear psychological triggers.

 

These patterns are consistent with emerging literature on toxicant-induced emotional dysregulation, and molecularly driven suicidality in post-TBI and chemically exposed populations. Yet, the healthcare system continues to respond with psychotropic polypharmacy, institutionalization, or administrative separation - rather than mechanism-aware diagnostics or exposure-informed care.

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The resulting profile includes REM Sleep Behavior Disorder (RBD), panic-like autonomic storms, mood dysregulation, executive flattening, all rooted in neuroinflammatory priming, dopaminergic signaling collapse, and limbic-cortical suppression.

 

Rather than isolate mental health as a standalone discipline, this chapter situates psychological symptoms within a broader syndrome of bioenergetic and synaptic dysfunction—a neurotoxic emotional dysregulation syndrome. The clinical features seen in the survivor are not abstract or speculative; they are molecular footprints, mirrored in literature, modeled in omics, and mapped across countless unrecognized lives.

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Clinical Mental Health Profile of the Survivor

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  • REM Sleep Behavior Disorder (RBD) with dream enactment

     

  • Episodic dysphoria with sudden mood shifts, often tied to fatigue or circadian disruption

     

  • Cognitive flattening and loss of affective nuance

     

  • Panic-like autonomic storms without psychological fear resulting in heart rate from stable to suddenly tachycardic shifting to bradycardia with or without hyper-vigilance

     

  • Emotional detachment during sensory overload

     

  • Nighttime parasomnias with vocalization and motor activity

     

  • Social withdrawal (post-insult anhedonia)

     

  • Hyper-vigilance

     

  • PTSD

     

  • Chemically Induced Depression

     

  • Chemically Induced Proclivity to Addiction

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Additional Clinical Presentation Common to Others

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  • Suicidal ideation, especially during neuroenergetic crashes

     

  • Decrease in Empathy

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Neurobiological Pathways of Injury

 

 

1. Limbic System Inflammation

Permethrin exposure primes microglia, the brain's immune cells, in key limbic regions like the amygdala and hippocampus. Microglial activation leads to the release of inflammatory cytokines, which disrupt the delicate neurochemical balance necessary for affective regulation. In these areas, crucial for fear modulation, empathy, and memory, this inflammatory cascade contributes to the emotional volatility experienced by most, though for our survivor this is limited to social detachment, and observed cognitive deficits compared to pre-exposure abilities.

 

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2. Endocannabinoid System (ECS) Suppression

The ECS is crucial for fear extinction, mood stabilization, and recovery from trauma. Suppressed ECS tone leaves the brain in a persistent state of alarm. This is visible in our survivor's flattened affect followed by emotional collapse - often mislabeled as psychosomatic,  pathological diagnosis driven by outdated diagnostic guidelines and limited review of patient data and history.  All of it simply to work within the comfort zone of a practitioner's existing knowledge and protocols - ignoring the mountain of data presented or available to them which would lead to better care - reinforcing academic, clinical, and social stigma. 

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3. Serotonergic and Dopaminergic Dysregulation

Permethrin-induced Nurr1 suppression and altered monoamine signaling, as observed in animal models, provide a plausible biological mechanism for the anhedonia, memory lapses, and REM dysfunction experienced by the survivor. In his case, these neurological imbalances emerged without a prior history of psychiatric illness, strongly suggesting a causal link to the constellation of exposures that include: being compelled to wear the prototype; subsequent injury; institutional abandonment over 20 years and four days; PTSD arising from assault; and a vehicular accident with resulting mTBI and concussion syndromes.

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4. Mitochondrial Collapse and Emotional Regulation Failure

When mitochondrial ATP generation falters, particularly in the prefrontal cortex, the brain's capacity for  "braking" is compromised. The Survivor's NAD+ depletion and increasing periods of executive instability are consistent with this system-wide energy failure, where the brain lacks sufficient energy to regulate responses effectively.

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5. Epigenetic Scarring Post-TBI

As research by Wong and Langley (2016) has shown, TBI can leave a lasting epigenetic scar on the brain. In survivors with prior chemical exposure, this epigenetic disruption can accelerate synaptic loss and further impair focus, memory, and emotional regulatory circuits, including BDNF expression.

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Reclaiming the Narrative for Those We Lost

 

 

The veteran suicide epidemic cannot be understood through psychological frameworks alone. Many who took their lives showed signs of:

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  • Sudden emotional fragmentation following field exposure

     

  • Autonomic instability mislabeled as panic

     

  • Treatment-resistant mood disorders that worsened with benzodiazepines (Ativan, Clonazepam) owing to the mechanisms of injury that harmed benzodiapine, gaba, and dopamine pathways.

     

  • Nightmares and RBD unresponsive to trauma therapy and prescribed interventions

 

 

 

These were not moral failings or personality defects. They were neurochemical injuries left unmeasured.

 

BioSymphony urges a diagnostic reclassification - not to erase suffering, but to see it clearly, to ground it in data, and to intervene with both trauma-based and toxic exposure aware care.

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Chapter 12. Literature Review

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​Neurochemical Destabilization, Epigenetic Imprinting, and the Psychiatric Misreading of Chemical Injury
 

 

Overview

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Mental health outcomes in toxicant-exposed individuals - particularly veterans - are often misunderstood, miscategorized, or dismissed entirely. All the more if that veteran is a woman.

 

What appears as psychiatric fragility or inherited mood disorder is, in many cases, the biochemical fingerprint of chronic chemical exposure layered atop trauma, circadian disruption, and neuroimmune injury.

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In this chapter, we examine the molecular, epigenetic, and behavioral effects of exposure to pyrethroids (including permethrin) and DEET. We trace these effects from microglial activation and dopaminergic instability to altered synaptic plasticity, HPA axis disturbance, and emotional dysregulation. Drawing from over a dozen peer-reviewed studies, we map a direct path from environmental toxicants to mood disorders - using the Survivor’s case as a lens to understand the hidden neuropsychiatric cost of chemically burdened service.

 

The evidence makes one thing clear:


What’s being misread as mental illness is, in many cases, mitochondrial, inflammatory, and molecular injury in disguise.

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Pyrethroid Exposure and Mood Disorders

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Emerging population-level data confirm that exposure to pyrethroids - common insecticides found in military-treated uniforms, household repellents, and agricultural applications - is significantly associated with depressive symptoms and cognitive decline. A 2023 NHANES-based study by Li et al. found that urinary levels of 3-PBA, a primary metabolite of pyrethroids, were positively correlated with increased incidence of depression in adults, even after adjusting for confounders (Li et al. 2023). Notably, the effect size was greater among those with lower physical activity - suggesting a possible mitochondrial or inflammatory mediation pathway.

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The Survivor’s history of energy collapse, REM parasomnias, and emotional flatlining after uniform exposure aligns with these findings. What appears as “atypical depression” in a psychiatric chart may, in truth, reflect disrupted neurotransmitter synthesis and neuroimmune signaling driven by pyrethroid exposure.

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Animal models echo this mechanism. In a landmark study by Gargouri et al., rats exposed to bifenthrin daily for 60 days developed depression-like behaviors, including increased despair behavior in the Forced Swim Test. Hippocampal assays revealed reduced acetylcholinesterase (AChE) activity and orphan nuclear receptor (Nurr1) suppression - critical for both cholinergic tone and inflammatory control. These animals also showed downregulation of muscarinic and nicotinic acetylcholine receptors, further compromising memory, emotion, and stress regulation. These aren’t subtle findings; they are foundational disruptions of affective neurobiology.

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DEET’s Neurological and Endocrine Disruption

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DEET, another chemical widely used by the military in combination with permethrin, also poses a silent threat to mental health, particularly during early development and adolescence. A 2025 cross-sectional analysis by Zhu et al. revealed that higher urinary levels of DCBA - a DEET metabolite - were linked to reduced testosterone and estrogen levels, elevated sex hormone-binding globulin (SHBG), and reduced bone mineral content in children under 12. The hormonal disturbances were even more pronounced in non-overweight participants, suggesting that leaner individuals may be more biochemically vulnerable (Zhu et al. 2025).

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The hormonal axis is tightly intertwined with the neuroendocrine system - especially in the context of mood, memory, and reward processing. Sudden shifts in estrogen, testosterone, and cortisol availability can destabilize mood, exacerbate fatigue, and alter synaptic pruning during neurodevelopment. These findings provide further support for viewing chemically induced endocrine dysfunction as a root contributor to psychiatric misdiagnosis - especially in veterans and youth exposed before or during puberty.

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DEET does not just affect the endocrine system - it  also disturbs mitochondrial energetics, glutamate signaling, and the GABAergic balance that governs mood.

 

In combination with pyrethroids like permethrin, this creates a neurochemical environment primed for dysregulation, even without psychological trauma.

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Neuroinflammation, Nurr1 Suppression, and Mitochondrial Collapse

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What links the Survivor’s symptoms - emotional bluntness, REM intrusion, dysphoria surges, and parasympathetic storms - is not a psychiatric syndrome. It is a chemically induced neurotoxicity emotional dysregulation syndrome brought on by  

neuroinflammation and mitochondrial collapse.  Suppression of Nurr1 has been linked to increased oxidative stress and dopaminergic degeneration in both rodent and postmortem human studies. When mitochondrial ATP generation falters, emotional control, memory, and autonomic regulation all degrade. This is not theoretical; it’s functional failure of the brain’s energetic and inflammatory equilibrium.(Gargouri et al. 2019; Antonangeli et al. 2023).

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Antonangeli et al. reviewed this dynamic in 2023, citing evidence that low-dose chronic pesticide exposure alters glial reactivity, cytokine signaling, and behavior even in the absence of overt neurological disease.⁵ In other words: you don’t need to “look sick” to be injured. The molecular changes are often invisible on imaging but have significant impact in daily life.

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These disruptions impact more than mood. They affect the limbic system’s ability to filter threat from safety, reward from punishment, and effort from exhaustion. In the Survivor, we see classic signs of baroreflex instability and mitochondrial collapse under exertion: dizziness, nausea, visual aura, followed by parasympathetic rebound and profound fatigue. These are not panic attacks. They are energy failures.

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Psychiatric Mislabeling and the Veteran Suicide Crisis

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One of the most heartbreaking consequences of these chemical injuries is the risk of mislabeling - especially in military and marginalized populations. Studies of Thai farmers and European agricultural workers show elevated suicide risk among those with long-term pesticide exposure, even after controlling for social and economic variables (Ong-Artborirak et al. 2022). These patterns mirror what we see in the Veteran community: high suicide rates, complex PTSD diagnoses, and emotional lability without adequate toxicological context.

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To treat chemically injured individuals as if their symptoms originate in the psyche rather than the synapse is not only misguided - it’s potentially lethal. It creates a loop of misdiagnosis, mistreatment, and medical gaslighting that drives despair deeper into the nervous system.

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For the Survivor, this misreading has real stakes. Being told that your despair over toxic polyneuropathy and lack of attention to degenerative neurocardiogenic disease is internal, inherited, or emotional and not being able to convince physicians that this a downstream effect of toxic exposure - when it is in fact biochemical and induced - can lead to hopelessness, stigma, and misaligned treatment. In the absence of toxin-informed care, veterans are too often medicated, marginalized, or left to self-medicate, with the root cause of their injury persisting without proper interventions. Many don’t survive.

 

Pyrethroid Exposure causation for ADHD in children and adults. 

 

Pyrethroid exposure's ability to trigger or exacerbate ADHD is a growing area of concern, with evidence emerging from both U.S. and European studies. Wagner-Schuman et al. (2015) in their nationally representative U.S. study, "Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children," demonstrated a significant association between pyrethroid exposure and ADHD, particularly hyperactive-impulsive symptoms. This crucial finding builds upon animal research that has repeatedly shown pyrethroids can disrupt the dopamine system and induce ADHD-like behaviors.

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This research gains further weight from a 2024 European study (Purece et al.), "Environmental burden of disease related to pyrethroid-insecticide exposure and neurodevelopmental toxicity in Europe based on human biomonitoring." This study, encompassing data from France, Germany, Iceland, Switzerland, and Israel, revealed widespread pyrethroid exposure in European children, often at higher levels than in adults, and calculated that a substantial number of ADHD cases (averaging 18%) can be attributed to this exposure. The authors quantified the potential health burden using disability-adjusted life years (DALYs), underscoring the significant public health implications.   

 

The body of evidence reviewed in our research, and that of peer-reviewed studies, raise significant concerns about the neurobehavioral effects of various insecticides, with particular attention drawn to pyrethroids and DEET. Research indicates a notable association between pyrethroid exposure in children and an elevated risk of ADHD, especially the hyperactive-impulsive subtype, with some studies suggesting that these effects may be more pronounced in boys. Furthermore, studies have linked residential pyrethroid exposure to an increased likelihood of depression and anxiety diagnoses in older adults, and there is even evidence pointing to a correlation between pyrethroid exposure and increased all-cause and cardiovascular mortality risk.   

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Beyond pyrethroids, animal studies have also demonstrated potential for DEET to cause significant neurotoxicity, with findings indicating that frequent and prolonged use of this chemical can lead to brain cell death and behavioral changes.   

 

Converging evidence highlights the importance of considering the long-term neurological consequences of exposure to both pyrethroids and other commonly used insecticides.

 

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Study Shows Link Between Pesticides and Increased Vulnerability to Depression

 

The study by Furlong et al. (2020), poignantly titled "Ambient Pyrethroid Pesticide Exposures in Adult Life and Depression in Older Residents of California's Central Valley," delves into a deeply concerning connection: the potential for everyday exposure to pyrethroid pesticides to contribute to the debilitating reality of depression in older adults. Their research offers compelling evidence, suggesting that these seemingly innocuous exposures may not be benign, but rather a significant factor in the development of this devastating condition.

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The findings of Furlong et al. (2020) resonate with the documented experience, contemporaneous notes, and clinical data of our survivor and others subjected to similar exposures. For the survivor, compelled to endure 52 consecutive days of wearing a prototype U.S. Army combat uniform laced with permethrin (at a concentration of 0.125 mg/cm²) under the extreme conditions of simulated expeditionary settings, intense heat, high humidity, and relentless physical exertion, this research illuminates a biological pathway for the subsequent development of depressive symptoms. While focused on ambient environmental exposures, this study lends significant scientific weight to the reality that sustained, high-level permethrin exposure, such as endured by many of our Armed Forces, directly contributes to the profound and enduring neuropsychiatric, chemical, and structural injury they suffer.

 

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Clinician’s Reframe

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It is time for psychiatry and primary care to shift from trauma-informed care alone to ensure the inclusion of toxin-informed diagnostics. For chemically exposed populations, the presence of mood disruption, anhedonia, anxiety surges, or REM parasomnias should not prompt SSRIs as a first-line response. It should prompt toxicological inquiry, mitochondrial screening, and neuroimmune profiling.

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Veterans who “don’t respond to treatment” may not be treatment-resistant - they may be injury-misdiagnosed. When we reframe their symptoms as the logical outcome of molecular insult, the path to effective care becomes clearer.

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What’s been dismissed as dysfunction is often the body’s attempt to survive in a poisoned system. 

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For the chemically exposed patient, what looks like panic may be baroreflex failure.


What looks like depression may be mitochondrial signaling collapse.


What looks like addiction may be a desperate attempt to self-stabilize a dysregulated system.

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The clinical frame must evolve. “Treatment resistance” may not be resistance at all - it may be a mismatch between the origin of the symptoms and the tools we’ve chosen to treat them.

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We don’t need to reinvent psychiatry.
We need to realign it with biology in combination with past and present occupational and environmental hazards. 

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Summary Insight

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The evidence is no longer circumstantial. It is molecular. Pyrethroids and DEET alter key neurochemical and hormonal pathways that govern mood, cognition, and stress response. In animal models, these changes lead to despair behaviors and structural brain changes. In humans, they manifest as fatigue, emotional dysregulation, and suicidality—especially in those with prior trauma or neurological injury.

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It is no coincidence that those most affected are veterans, agricultural workers, and the chemically injured. These are not broken minds. These are wounded systems.

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And they deserve more than prescriptions. They deserve recognition, reparative care, and the protection of science that does not look away.

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