The cells aren't deficient. They can't use what we give them.
MCAS. Mercury toxicity. B12 deficiency. Copper imbalance. They're treated as separate conditions. They're all the same underlying crisis.
Transport failure is the root.
Mercury hijacks DMT1 - the divalent metal transporter - blocking iron uptake while increasing toxic metal accumulation.
Anti-CD320 autoantibodies cause B12 deficiency despite normal serum levels. The B12 is there. It just can't get into cells.
Under inflammatory stress, copper transport efficiency drops by 50%. You can have elevated ceruloplasmin while experiencing functional copper deficiency.
When inflammation downregulates transporter families through shared pathways, multiple "deficiencies" appear simultaneously. Not because nutrients are missing. Because they can't get where they need to go.
Minerals aren't deficient. They're imprisoned.
Chronic inflammation triggers IL-6 and TNF-α, which drive hepcidin overproduction.
Hepcidin binds ferroportin and degrades it within 3-6 hours, trapping iron in macrophages and enterocytes.
High ferritin, low serum iron. The classic "anemia of chronic disease."
Hepcidin reduces zinc transport. Inflammation increases liver sequestration by 3.5x.
Metallothionein increases up to 35-fold, binding all available metals.
Studies with hepcidin antagonists show rapid mineral mobilization without supplementation. The minerals were never deficient. They were locked away.
Bile connects everything.
Bile acids directly trigger mast cell degranulation at physiological concentrations. This creates a self-perpetuating cycle.
The alpha-gal connection is revealing. Alpha-gal bound to lipids triggers systemic reactions. These glycolipids require bile acid micelles for absorption.
This explains the 3-6 hour delay in alpha-gal reactions - it matches lipid digestion timing.
Cells get stuck in defense mode.
When cells detect threats exceeding their capacity - mercury, infections, immune challenges - they shift from normal metabolism to defensive mode.
Inflammatory containment
Proliferation
Healing/reintegration
In chronic illness, cells get stuck in CDR1 or CDR2. They can't progress to healing. Nutrient transport shuts down. Biosynthesis stops. This creates apparent deficiencies despite adequate serum levels.
Pseudodeficiency changes everything.
The distinction between true deficiency and functional deficiency from transport failure fundamentally changes treatment.
Up to 45% of patients with functional B12 deficiency show normal serum levels. Only elevated methylmalonic acid reveals the cellular dysfunction.
Ferritin over 500 ng/mL with transferrin saturation under 20% = iron is present but sequestered.
Resistance requiring supraphysiologic doses = receptor dysfunction, not deficiency.
Aggressive supplementation can make things worse - competitive inhibition, transport saturation, increased oxidative stress. Addressing root causes works better.
Stop chasing deficiencies. Start addressing the system.
Restore cellular transport
Reduce inflammation - this releases sequestered minerals. IL-6 antagonists improve mineral status. Zonulin inhibitors reduce permeability.
Exit the Cell Danger Response
Remove triggers - heavy metals, infections, allergens. Support mitochondrial membrane repair. Let cells perceive safety so they can exit defense mode.
Fix bile acid metabolism
Support bile flow - this affects everything. Modulate mast cell activation. Support beneficial gut bacteria for proper bile acid transformation.
The cells aren't broken. They're defending themselves.
Transport proteins fail. Minerals get sequestered. Cells enter protective shutdown. Apparent deficiencies appear despite adequate supply.
Help them feel safe enough to stand down.