Case Report: Full Ecological Collapse and Systemic Failure
This is a long, structured case report documenting a collapse-pattern trajectory and protocol transition; posting for documentation and shared learning.
Contents:
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Background and Helminth Stability
I lived with a long-standing autoimmune condition that remained non-symptomatic for five years with helminthic therapy. During that time, regulation was successful enough for me to go from bedridden to fully functional. Helminths consistently maintained immune balance and kept inflammation controlled.
Iron Infusions and Systemic Failure
In late 2023, an iron infusion produced an autoimmune flare that resolved after a few weeks. In early 2024, a second infusion caused another flare, but this time the consequences were qualitatively different: chronic hives, MCAS-type reactivity, new rheumatoid-arthritis manifestations including bent fingers and swollen joints, and significant fatigue. I became bedridden again for a period. The system, previously regulated, had become unstable.
Full Ecological Collapse
Unable to determine whether the hives were driven by diet, supplements, or something else, I ordered a shotgun metagenomics test in August 2024. The results were so extreme that I went into denial. I changed my diet, increased fiber, and added probiotics along with other standard dysbiosis-oriented strategies. None of these interventions altered the ecological pattern. A repeat test earlier this summer confirmed no improvement.
At that point I accepted that the system was not dysbiotic but in full ecological collapse. Helminths were no longer able to regulate it because the mucosal barrier was too degraded, the endotoxin load too high, and the signaling environment too disordered for helminthic immune-modulation to overcome. The dynamic resembled trying to extinguish a fire while adding fuel to it.
DBKR Sequence and Pause-Week Failure
The stool data showed Proteobacteria and Enterobacteriaceae dominance of 70–80%. These organisms—Enterobacter, E. coli, Klebsiella, Pseudomonas, Burkholderia, Ralstonia—are efficient iron scavengers and thrive in oxygenated micro-niches. The iron infusions initiated the bloom, but the collapse-pattern now sustains them without ongoing iron exposure. Biofilm-producing Enterobacteriaceae create micro-aerobic pockets and exclude anaerobes. The test data placed Pseudomonas, Ralstonia, and Burkholderia at the 99.9th percentile. By contrast, butyrate producers were nearly absent: Akkermansia at 0.0003%, Roseburia at 0.03%, and Faecalibacterium at 0.25%. Permeability and inflammation were high. Systemically, this translated into elevated ROS, mitochondrial stress, and energy instability.
On October 1, I began a disrupt → kill → bind → restore sequence resembling DBKR logic, using enzymes, biofilm chelators, and high-potency antimicrobials aimed at reducing Enterobacteriaceae dominance. This was followed by binders and post-antimicrobial support intended to stabilize bile acids, reduce endotoxin load, and prepare the environment for repair.
DBKR incorporated a pause week to avoid antimicrobial resistance. The pause ended October 28. Symptoms returned rapidly during the pause, and resuming antimicrobials did not restore previous stability. This made it clear that the earlier apparent improvements reflected suppression rather than recovery. The system reverted immediately when pressure lifted, indicating that the underlying forces of collapse remained intact.
Identification of Collapse-Pattern Forces
This was the pivot point. It became clear that the situation was not “dysbiosis” and not amenable to a sequential disrupt/kill/repair logic. The problem was a collapse-pattern maintained by interlocking forces: permeability, bile-acid epithelial injury, mitochondrial ROS load, ENS hyperexcitation, and mucin depletion. These forces formed a self-sustaining loop. Iron had been the triggering event in 2023–2024, but iron was no longer the driver. The collapse-pattern itself had become the stabilizing architecture.
DBKR was structurally incapable of unwinding this. It targets organisms rather than forces. The kill-phase aggravated fragility by destabilizing the small amount of regulatory tone that remained. The repair-phase presupposed mitochondrial, mucin, bile, and neural stability that was not present. Anaerobic niches were absent, making recolonization impossible. Biofilm-stabilized micro-aerobic niches favored persistence of Enterobacteriaceae. The pause-week failure was functional confirmation that DBKR could not restore this system.
Interim Stabilizers
I discontinued DBKR and reinstalled helminths on November 4. They now provide limited regulatory signaling but cannot override collapse-pattern pressures because permeability, mucin loss, and ROS have made the environment non-responsive to helminth-driven Treg signaling. Hydroxychloroquine adds partial immune modulation, and prednisone is required intermittently for symptom control. These three—helminths, HCQ, and intermittent prednisone—are the only active stabilizers at this point.
I stopped all destabilizing interventions and focused on correcting the protocol design; aside from HCl with meals, the system is unchanged while I assemble the components needed to begin Gate. During this period, I realized that the NAD precursor in the nearly finalized protocol might be a mismatch. Further investigation confirmed that NR is poorly suited to a Proteobacteria-dominant ecology because it requires bacterial deamidation, is vulnerable to microbial uptake, and would likely not reach host tissues in this collapse-pattern. I corrected this to niacinamide in the individualized protocol plan.
Development of the Gate Protocol
During November, I completed development of an individualized protocol based on the Gate architecture. This required mapping collapse-pattern drivers, assigning interventions to pressure nodes, and building a staged sequence aligned with dependencies across immune alarm, mitochondrial ROS, bile toxicity, ENS activation, and mucin restoration. Apart from the NAD precursor correction, no other structural mismatches are currently apparent.
Gate Initiation Plan
I will begin Gate in mid-December using the components currently available. Gate is a method for sequentially unwinding collapse-pattern forces rather than targeting organisms. Additional tools—photobiomodulation arriving mid-January, peptides still in transit, and possibly phages after the next test—will be integrated later. Early Gate is not oriented toward recolonization. Its function is to reduce pressure across epithelial, mitochondrial, bile-acid, and neural systems to create viability for later ecological recovery.
Timeline and Next Steps
The next shotgun metagenomics test will be scheduled for March 1 to allow sufficient time in Gate-stabilized conditions. The retest will assess Enterobacteriaceae burden, anaerobic potential, bile patterns, mucin-adjacent commensals, and SCFA capacity. These findings will determine the direction of the next phase, including possible use of targeted phages.
This is an interim case report documenting the transition from a DBKR sequence to a collapse-pattern architecture. Although I corrected a major mechanistic mismatch (the NAD precursor issue), additional mismatches remain possible and will be re-evaluated after the next metagenomics results.
This is a long, structured case report documenting a collapse-pattern trajectory and protocol transition; posting for documentation and shared learning.
Contents:
- Background and Helminth Stability
- Iron Infusions and Systemic Failure
- Full Ecological Collapse
- DBKR Sequence and Pause-Week Failure
- Identification of Collapse-Pattern Forces
- Interim Stabilizers
- Development of the Gate Protocol
- Gate Initiation Plan
- Timeline and Next Steps
----------------------------------------
Background and Helminth Stability
I lived with a long-standing autoimmune condition that remained non-symptomatic for five years with helminthic therapy. During that time, regulation was successful enough for me to go from bedridden to fully functional. Helminths consistently maintained immune balance and kept inflammation controlled.
Iron Infusions and Systemic Failure
In late 2023, an iron infusion produced an autoimmune flare that resolved after a few weeks. In early 2024, a second infusion caused another flare, but this time the consequences were qualitatively different: chronic hives, MCAS-type reactivity, new rheumatoid-arthritis manifestations including bent fingers and swollen joints, and significant fatigue. I became bedridden again for a period. The system, previously regulated, had become unstable.
Full Ecological Collapse
Unable to determine whether the hives were driven by diet, supplements, or something else, I ordered a shotgun metagenomics test in August 2024. The results were so extreme that I went into denial. I changed my diet, increased fiber, and added probiotics along with other standard dysbiosis-oriented strategies. None of these interventions altered the ecological pattern. A repeat test earlier this summer confirmed no improvement.
At that point I accepted that the system was not dysbiotic but in full ecological collapse. Helminths were no longer able to regulate it because the mucosal barrier was too degraded, the endotoxin load too high, and the signaling environment too disordered for helminthic immune-modulation to overcome. The dynamic resembled trying to extinguish a fire while adding fuel to it.
DBKR Sequence and Pause-Week Failure
The stool data showed Proteobacteria and Enterobacteriaceae dominance of 70–80%. These organisms—Enterobacter, E. coli, Klebsiella, Pseudomonas, Burkholderia, Ralstonia—are efficient iron scavengers and thrive in oxygenated micro-niches. The iron infusions initiated the bloom, but the collapse-pattern now sustains them without ongoing iron exposure. Biofilm-producing Enterobacteriaceae create micro-aerobic pockets and exclude anaerobes. The test data placed Pseudomonas, Ralstonia, and Burkholderia at the 99.9th percentile. By contrast, butyrate producers were nearly absent: Akkermansia at 0.0003%, Roseburia at 0.03%, and Faecalibacterium at 0.25%. Permeability and inflammation were high. Systemically, this translated into elevated ROS, mitochondrial stress, and energy instability.
On October 1, I began a disrupt → kill → bind → restore sequence resembling DBKR logic, using enzymes, biofilm chelators, and high-potency antimicrobials aimed at reducing Enterobacteriaceae dominance. This was followed by binders and post-antimicrobial support intended to stabilize bile acids, reduce endotoxin load, and prepare the environment for repair.
DBKR incorporated a pause week to avoid antimicrobial resistance. The pause ended October 28. Symptoms returned rapidly during the pause, and resuming antimicrobials did not restore previous stability. This made it clear that the earlier apparent improvements reflected suppression rather than recovery. The system reverted immediately when pressure lifted, indicating that the underlying forces of collapse remained intact.
Identification of Collapse-Pattern Forces
This was the pivot point. It became clear that the situation was not “dysbiosis” and not amenable to a sequential disrupt/kill/repair logic. The problem was a collapse-pattern maintained by interlocking forces: permeability, bile-acid epithelial injury, mitochondrial ROS load, ENS hyperexcitation, and mucin depletion. These forces formed a self-sustaining loop. Iron had been the triggering event in 2023–2024, but iron was no longer the driver. The collapse-pattern itself had become the stabilizing architecture.
DBKR was structurally incapable of unwinding this. It targets organisms rather than forces. The kill-phase aggravated fragility by destabilizing the small amount of regulatory tone that remained. The repair-phase presupposed mitochondrial, mucin, bile, and neural stability that was not present. Anaerobic niches were absent, making recolonization impossible. Biofilm-stabilized micro-aerobic niches favored persistence of Enterobacteriaceae. The pause-week failure was functional confirmation that DBKR could not restore this system.
Interim Stabilizers
I discontinued DBKR and reinstalled helminths on November 4. They now provide limited regulatory signaling but cannot override collapse-pattern pressures because permeability, mucin loss, and ROS have made the environment non-responsive to helminth-driven Treg signaling. Hydroxychloroquine adds partial immune modulation, and prednisone is required intermittently for symptom control. These three—helminths, HCQ, and intermittent prednisone—are the only active stabilizers at this point.
I stopped all destabilizing interventions and focused on correcting the protocol design; aside from HCl with meals, the system is unchanged while I assemble the components needed to begin Gate. During this period, I realized that the NAD precursor in the nearly finalized protocol might be a mismatch. Further investigation confirmed that NR is poorly suited to a Proteobacteria-dominant ecology because it requires bacterial deamidation, is vulnerable to microbial uptake, and would likely not reach host tissues in this collapse-pattern. I corrected this to niacinamide in the individualized protocol plan.
Development of the Gate Protocol
During November, I completed development of an individualized protocol based on the Gate architecture. This required mapping collapse-pattern drivers, assigning interventions to pressure nodes, and building a staged sequence aligned with dependencies across immune alarm, mitochondrial ROS, bile toxicity, ENS activation, and mucin restoration. Apart from the NAD precursor correction, no other structural mismatches are currently apparent.
Gate Initiation Plan
I will begin Gate in mid-December using the components currently available. Gate is a method for sequentially unwinding collapse-pattern forces rather than targeting organisms. Additional tools—photobiomodulation arriving mid-January, peptides still in transit, and possibly phages after the next test—will be integrated later. Early Gate is not oriented toward recolonization. Its function is to reduce pressure across epithelial, mitochondrial, bile-acid, and neural systems to create viability for later ecological recovery.
Timeline and Next Steps
The next shotgun metagenomics test will be scheduled for March 1 to allow sufficient time in Gate-stabilized conditions. The retest will assess Enterobacteriaceae burden, anaerobic potential, bile patterns, mucin-adjacent commensals, and SCFA capacity. These findings will determine the direction of the next phase, including possible use of targeted phages.
This is an interim case report documenting the transition from a DBKR sequence to a collapse-pattern architecture. Although I corrected a major mechanistic mismatch (the NAD precursor issue), additional mismatches remain possible and will be re-evaluated after the next metagenomics results.