The pathological disruption of normal metal homeostasis — the tightly regulated balance of essential trace elements (iron, zinc, copper, manganese, selenium) and exclusion of toxic metals (cadmium, lead, mercury, arsenic). Dyshomeostasis is a convergent mechanism underlying nearly every disease in this wiki.
Manifestations
- Excess: iron overload (ferroptosis), copper accumulation (Wilson disease), manganese toxicity (manganism).
- Deficiency: zinc deficiency (immune dysfunction, growth retardation), selenium deficiency (thyroid dysfunction, Keshan disease), iron deficiency (anemia).
- Redistribution: metals may be globally adequate but locally mislocalized (e.g., iron accumulation in substantia nigra during parkinsons disease despite systemic adequacy).
- Ratio disruption: Cu:Zn ratio elevation is documented in colorectal cancer, cardiovascular disease, pcos, and inflammation.
Microbiome Connections
- Gut bacteria modulate metal absorption, speciation, and systemic distribution.
- dysbiosis both causes and results from metal dyshomeostasis — a bidirectional feedback loop.
- The gut metal microbiome axis is where dietary metal exposure first encounters microbial modifiers.
Connections
- gut metal microbiome — the ecosystem where dyshomeostasis originates
- nutritional immunity — host-imposed metal restriction as antimicrobial defense
- oxidative stress — dyshomeostasis drives ROS generation via Fenton/Haber-Weiss chemistry
- metal disease matrix — maps dyshomeostasis patterns across diseases
- inflammation — bidirectional relationship with metal imbalance