been down a rabbit hole since that GLP-1/hallmarks-of-aging thread a few days ago and genuinely curious what people here think. the distinction that keeps nagging at me: the LEV Foundation framing around mouse rejuvenation is explicitly about reversing biological age - not just reducing damage accumulation or metabolic stress, but actual rollback. the mechanism language is different from what you see in GLP-1 literature, where the favorable signal is mostly “less chronic stress on the system” rather than “we turned something back.” which makes me wonder if people are actually building stacks with those as separate goals, or if they’re collapsing into each other in practice. like - if you’re on sema or tirz already (metabolic load down, inflammation markers improving, glucose stable), and you want to layer in something with a more explicit rejuvenation aim, what are you actually adding? i’ve seen rapamycin, NAD precursors, senolytics mentioned in passing. some peptides with MOTS-c / epitalon framing. but i’m skeptical of the translation from the mouse data and i’d want to know: are the people actually running these stacks treating the GLP-1 as the foundation and adding on top, or are they running them independently? also genuinely asking bc the postpartum + sleep-deprived + 35 context probably matters for risk tolerance here - the senolytic literature in particular has “do not mess with this casually” vibes. what are people actually doing, and how are you thinking about the distinction?