Johanna Ihli, BSN
Former Registered Nurse (Emergency, Trauma, and Critical Care)
Independent Researcher in Drug-Induced Mitochondrial Dysfunction
ORCID: https://orcid.org/0009-0008-1486-7242
How I Got Here
For more than three decades, I lived inside medicine—first as a registered nurse working in emergency, trauma, and critical care, and later as a patient navigating an increasingly fragmented healthcare system while experiencing progressive, unexplained multisystem decline.
I survived two fluoroquinolone antibiotic exposures separated by nearly twenty years. What followed was not a single diagnosis or isolated event, but a slow cascade of injuries unfolding over time and across body systems: spontaneous tendon ruptures, muscle spasms, progressive neuropathy, autonomic instability, gait changes, unexplained rashes, visual impairment, insomnia, cognitive and psychological changes, and profound, accumulating fatigue.
Like many patients with complex, delayed injury patterns, I was referred from specialist to specialist. Each evaluated the system they knew best and ruled out what they could see. No one was trained—or incentivized—to look for a unifying mechanism beneath the surface. Standard care during these encounters often involved corticosteroids and NSAIDs, medications now known to worsen mitochondrial dysfunction. Rather than improvement, these interventions were followed by progressive clinical deterioration.
In 2025, comprehensive mitochondrial testing finally identified a Complex I deficiency, confirming long-suspected mitochondrial dysfunction. This result did not simply explain my current condition—it explained decades of delayed injury, partial recovery, compensation, and eventual structural failure.
Why This Matters
Mitochondria are not an abstract concept reserved for rare genetic diseases. They are the energetic foundation of every high-demand tissue in the human body. Their proper function is essential for cellular repair, signaling, and long-term resilience.
When mitochondrial function is impaired, injury does not always present immediately. Cells compensate. Systems adapt. Symptoms may remain sub clinical until physiologic thresholds are crossed—sometimes years or decades later.
Current clinical frameworks are poorly equipped to recognize this pattern.
Modern medicine is trained to identify discrete diagnoses, not cumulative cellular injury. Regulatory toxicity frameworks and FDA guidelines were largely established for acute, reversible, and time-limited reactions. Delayed mitochondrial toxicity—especially when it manifests across multiple systems—often falls outside these models and goes unrecognized.
This gap is not due to malice or neglect. It is structural. It is educational. It is systemic.
Background and Perspective
I bring both clinical training and personal experience to this work.
My background in emergency, trauma, and critical care provided firsthand insight into how care is delivered under pressure and within guideline-driven systems. My own experience with delayed, multisystem medication-related injury exposed the limitations of those systems when harm unfolds outside expected timelines or diagnostic categories.
With objective mitochondrial findings now available, my work is centered on recognition, prevention, and long-term accountability—so patients are not left without answers for years or decades.
The Purpose of This Site
This site exists to:
Document drug-induced mitochondrial dysfunction (DIMD) as a real, clinically relevant mechanism of injury
Translate complex mitochondrial science into language clinicians, patients, and policymakers can understand
Expose gaps in current diagnostic, regulatory, and surveillance frameworks
Support earlier recognition and prevention of delayed drug-related harm
Create infrastructure for education, research collaboration, and patient-reported data
This is not an anti-medicine project.
It is a pro-medicine, pro-science, pro-patient effort to modernize how we understand mitochondrial injury.
DIMD 