What to Fix First in a Protocol Where Senolytic Rebound Exceeds Your Proteasome Capacity
You ran your opened senolytic pulse — maybe dasatinib + quercetin, maybe fisetin. You expected a bounce in energy, clearer skin, maybe deeper sleep. Instead, you got joint stiffness, brain fog that won't quit, and a CRP that climbed. The rebound is real, and it's not 'healing crisis.' It's your proteasome clogged with apoptotic debri, and your lysosomes are backing up like a drain that never got a strainer. So what do you fix opened? The answer isn't 'more autophagy,' because if the proteasome is already saturated, cranking autophagy just piles on more half-digested junk. You have to triage the chokepoint. Here's how to think about it — without the usual supplement-bro logic. Where This Rebound Shows Up in Real Life The gut-brain axis as a primary responder Senolytic rebound doesn't announce itself like a clean lab graph.