Combining the quantitative lifespan formula L=Tavg ×N from SFL-LS-01 and the G₀−ΔGd cellular damage system in SFL-CELL serial, this paper confirms that the hematopoietic system acts as the core upstream foundation determining global Tavg and the consumption rate of fixed renewal quota N. Bone marrow hematopoietic stem cells carry the most critical G₀ functional modules governing platelet, blood cell and microvascular repair capacity, consistent with the platelet repair dysfunction pathogenesis elaborated in SFL-CELL-02. Severe irreversible ΔGd(-) erosion of hematopoietic stem cell G₀ architecture produces structurally defective blood cells, fails to complete systemic microvascular repair continuously, accumulates massive tissue debris and triggers persistent pathological cellular turnover across the whole body, which directly compresses the average functional cycle Tavg of all somatic cells. Under the unified baseline N=10 for comparative deduction: individuals with intact bone marrow G₀ stability maintain Tavg=8 years and a theoretical lifespan of 80 years; once hematopoietic G₀ modules sustain long-term structural loss, systemic cell premature damage becomes universal, Tavg drops sharply and the fixed renewal quota N depletes rapidly. This paper distinguishes two layers of hematopoietic damage consequences: mild ΔGd accumulation only causes sub-health and recurrent mild inflammation; severe bone marrow G₀ collapse evolves into chronic inflammatory constitution such as SLE. All aging and lifespan consumption phenomena traced in subsequent SFL-LS papers ultimately trace back to the stability of the hematopoietic core pillar, building a bridge connecting the hematopoietic cellular pathology of SFL-CELL with the lifespan quantitative model of the LS series.
FOO SENG ANG (Sun,) studied this question.