To address this, we are pursuing three complementary lines of investigation: (i) dose–response studies in a Dex‐induced atrophy model with and without concurrent HFHS feeding; (ii) mechanistic testing in TLR4‐deficient mice, administering PSE or PCA to determine whether anti‐atrophic effects are mediated, at least in part, through TLR4‐linked inflammatory signaling; and (iii) efficacy studies in aged mice to evaluate PSE's ability to protect against age‐associated skeletal muscle atrophy and strength loss. Here, TLR4 is linked to Skeletal muscle atrophy.