Synthesizing the pathogenic mechanisms elaborated in SFL-CELL-02 to SFL-CELL-05, this paper integrates SLE, malignant tumors, ALS, Parkinson’s disease and Alzheimer’s disease into a single unified theoretical framework defined as the chronic disease repair decline spectrum, fully relying on the cellular G₀ and ΔGd axiom established in SFL-CELL-01. All human chronic disorders originate from the same root logic: irreversible ΔGd(−) damage erodes the fixed native G₀ functional modules of target cells, weakening intrinsic tissue repair capacity; persistent micro-damage cannot be fully cleared, and secondary inflammatory or proliferative abnormalities emerge as derivative symptoms, rather than independent primary illnesses. Universal state equation adopted by all branches of the SFL theoretical system G = G₀ + ΔGd(+) − ΔGd(−) Minor physiological abrasion ΔGd(+) is reversible and does not break normal tissue repair balance. When ΔGd(−) accumulates continuously in hematopoietic stem cells, somatic proliferative cells or central motor/protein-regulating neurons, the baseline functional value G of cells declines permanently, triggering distinct disease phenotypes corresponding to the impaired G₀ module. SLE stems from damaged platelet repair modules in bone marrow; tumors arise from collapsed proliferation restriction modules; ALS and cognitive degenerative diseases result from impaired nerve conduction and protein clearance modules respectively. Conventional medical research classifies these illnesses as unrelated independent conditions, yet they belong to different positions on one continuous repair decline spectrum differentiated only by cell type and damaged G₀ segment. Clinical treatments focused merely on suppressing inflammation, removing tumors or clearing protein deposits only relieve superficial manifestations. The universal fundamental therapeutic principle is to reduce external sources of ΔGd(−) damage and preserve the integrity of cellular native G₀ architecture. This unified spectrum connects all preceding CELL papers into a logically closed system, and the long-term whole-body aging consumption caused by persistent repair decline can be quantitatively calculated and predicted through the lifespan model presented in the subsequent SFL-LS serial.
FOO SENG ANG (Sat,) studied this question.