Dr. Autumn Frandsen, ND

Abstract

This case describes a 71-year-old female presenting with acute-onset neuropsychiatric and systemic symptoms following relocation to a new office environment. Laboratory evaluation revealed elevated complement component C4a and multi-class mycotoxin positivity, including markedly elevated ochratoxin A. Additional findings demonstrated mold-specific immune reactivity without a full chronic inflammatory response syndrome (CIRS) profile. Initial treatment with activated charcoal and phosphatidylcholine resulted in mild improvement and partial reduction in inflammatory markers. Subsequent addition of oral immunotherapy and L-theanine led to further improvement in neuropsychiatric symptoms. Escalation of binding therapy with a bile acid sequestrant resulted in substantial recovery over two months. Persistent insomnia resolved following titration of intravenous glutathione. This case highlights the importance of differentiating mycotoxin illness from CIRS and emphasizes the role of treatment sequencing in complex environmental illness.

Introduction

Mycotoxins are biologically active compounds capable of disrupting cellular membranes, impairing mitochondrial function, and altering immune signaling. Clinical manifestations may involve multiple systems, including neurological, gastrointestinal, and musculoskeletal domains.

Environmental illness exists along a spectrum. While chronic inflammatory response syndrome (CIRS) represents a well-described subset characterized by specific biomarker patterns and immune dysregulation, not all patients with mycotoxin exposure meet criteria for CIRS. Differentiating between these entities may have important implications for treatment strategy.

Case Presentation

A 71-year-old female with no prior psychiatric history presented with sudden onset of:

• Severe anxiety
• Insomnia
• Cognitive dysfunction
• Fatigue
• Severe neck and shoulder pain
• Abdominal pain
• New intolerance to previously well-tolerated foods

Symptoms began within months of moving into a new office building, suggesting a potential environmental trigger.

Differential Diagnosis

Considered etiologies included:

• Primary psychiatric disorder
• Neuroinflammatory or neurodegenerative disease
• Endocrine dysfunction
• Chronic infection (Lyme disease, EBV)
• Chronic inflammatory response syndrome (CIRS)
• Environmental toxin exposure (including mycotoxins)

The acute onset, lack of psychiatric history, and environmental correlation made a primary psychiatric etiology less likely.

Etiological Considerations

Mycotoxin exposure was suspected based on environmental timing and symptom pattern. Mycotoxins such as ochratoxin, gliotoxin, and trichothecenes are known to:

• Disrupt lipid membranes
• Induce oxidative stress
• Alter immune signaling
• Affect central nervous system function

In this case, both toxin burden and immune sensitization appeared to contribute to disease expression.

Diagnostic Assessment

Inflammatory and Regulatory Markers

• C4a: 5600 (elevated)
• TGF-β1: 7210 (markedly elevated)
• MMP-9: normal
• VEGF: normal
• MSH: normal
• ADH/osmolality: normal

Mycotoxin Testing

• Elevated ochratoxin A
• Elevated gliotoxin
• Presence of aflatoxins, trichothecenes, zearalenone 

• Lyme disease: negative
• Epstein Barr Virus: negative

Clinical Interpretation

Findings indicated:

• Significant toxin burden
• Partial inflammatory activation

The absence of widespread biomarker abnormalities suggested a non-CIRS mycotoxin illness with immune involvement.

CIRS vs Mycotoxin Illness

CIRS:

• Broad biomarker dysregulation
• Persistent innate immune activation

Non-CIRS Mycotoxin Illness:

• Selective biomarker abnormalities
• May include immune sensitization without full systemic dysregulation

This patient’s profile aligned with the latter.

Therapeutic Intervention

Initial Intervention: Binding and Membrane Support

• Activated charcoal 500 mg twice daily
• Phosphatidylcholine 300–600 mg daily

Clinical Response:

• Mild improvement in anxiety
• Mild cognitive improvement

Follow-Up Laboratory Assessment

After initial therapy:

• C4a decreased from 5600 → 3500
• TGF-β1 decreased from 7210 → 6500

These findings indicated partial reduction in inflammatory signaling, despite persistent symptoms.

At this time, mold IgE and IgG testing were performed to try to ascertain whether the persistent symptoms were exacerbated by consistent exposure, confirming significant immune sensitization.

Mold Immune Reactivity

IgE:

• Cladosporium herbarum: 2.4
• Penicillium chrysogen: 4.1
• Remaining panel: negative

IgG:

Broad elevation across multiple molds (including Cladosporium, Aspergillus, Setomelanomma, Curvularia)

• Clinical Interpretation of Findings Indicated: Strong mold-specific immune sensitization

Intermediate Intervention: Immune Modulation and Neuroregulation

• Oral immunotherapy (1 → 5 drops over 5 weeks)
• L-theanine 200 mg three times daily

Clinical Response:

• Substantial reduction in anxiety
• Improved cognitive clarity
• Improved emotional stability

Escalation of Binding Therapy

• Cholestyramine introduced

Clinical Response (2 months):

• Resolution of fatigue
• Resolution of pain
• Improved GI symptoms
• Reduced food intolerance

Final Intervention: Glutathione

• IV glutathione titrated from 1000 mg → 3000 mg over 6 weeks

Clinical Response:

• Resolution of insomnia

Outcome

• Neuropsychiatric symptoms resolved
• Systemic symptoms improved
• Sleep normalized

Discussion

Objective improvement may precede symptom resolution

Early reductions in C4a and TGF-β1 suggest physiologic improvement before full clinical recovery.

Immune sensitization can sustain symptoms

Persistent immune reactivity likely contributed to ongoing neuropsychiatric symptoms.

Neuroimmune dysregulation is central

Disrupted immune–nervous system communication likely played a key role.

Treatment sequencing is critical

Improvement followed staged progression:

1. Binding + membrane support
2. Immune modulation + neuroregulation
3. Enhanced binding
4. Antioxidant support

Glutathione as a late-stage intervention

Effective for residual symptoms once upstream processes were addressed.

Conclusion

This case demonstrates that mycotoxin-associated illness may present without a full CIRS biomarker profile and may require a staged therapeutic approach. Early improvements in inflammatory markers may not correspond to full symptom resolution when immune dysregulation persists. Addressing toxin burden, immune sensitization, and neuroregulation in sequence may optimize clinical outcomes.

Autumn Frandsen, ND is a licensed naturopathic physician specializing in environmental medicine, complex chronic illness, and toxin-mediated disease. She practices with the National Association of Environmental Medicine (NAEM), where she focuses on conditions such as mycotoxin illness, chronic inflammatory response syndromes, neuroimmune dysregulation, and environmentally acquired sensitivities.

Dr. Frandsen’s clinical approach integrates functional laboratory assessment, toxin-binding strategies, immune modulation, mitochondrial support, and individualized detoxification protocols. She has particular expertise in differentiating overlapping environmental and inflammatory conditions and applying structured, sequential treatment strategies to optimize patient outcomes.

She is committed to evidence-informed, systems-based care and to advancing clinician education in the recognition and treatment of environmentally driven illness, with an emphasis on restoring physiologic resilience and long-term health.

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