# Diet–Heart (Saturated Fat) Hypothesis

Saturated-for-cis-unsaturated replacement can raise LDL/apoB and is expected to raise ASCVD risk; the net clinical effect depends on the replacement, food matrix and exposure context.

Overall Ε follows preregistered SC3. The isolated biomarker component is Γ and the independently convergent particle-to-ASCVD component is Η. SC3 is assessed on their assembled complementary evidence with clinical dietary results, not by reimposing the biomarker cap on the whole set. Comparator-specific effects, historical endpoint conflicts, food matrix and uncertain selective mediation prevent broad diet-specific Ζ. This remains a bounded reviewer judgement, not a numerical estimate of individual risk.

Baseline metabolic state, fatty-acid species, cis-PUFA versus cis-MUFA, food matrix and duration map positive context boundaries. Carb replacement and multicomponent diet benefits address different contrasts. This is context-specific risk contribution, not universal mortality benefit.