Researcher6076
Explorer
Aloha All, In case anyone finds it useful: it has been 30 days since I took FOXO4-dri 28 mg 3x q48h. I'm writing everything down in a diary that I plan to publish on my website. So far there have been no adverse reactions. As for results, the lab tests are inconclusive at this point. The visible changes, however, leave no doubt that the dose was biologically active in my case. I am 71 yo, and the backs of my hands and my scalp used to carry widespread dark brown age spots. "Used to" is the key phrase here. By +30 days they have faded somewhere between more than 75% and 90%. A plausible sequence would be senescent-cell elimination → reduced melanogenic signaling → less new melanin production → existing melanin gradually moves outward with keratinocytes → shedding of pigmented keratinocytes → continued visible fading. The visual change is remarkable.
Given this visual evidence, the other changes below become likely rather than merely plausible.
Reduced SASP/inflammaging. Since SASP is able to trigger inflammation and even secondary senescence in cells nearby, eliminating its source may produce effects that persist far longer than the senolytic exposure itself.
Improved endothelial function. Over a period of weeks, endothelial remodeling could plausibly influence vascular elasticity, nitric-oxide biology and microvascular function.
Reduced propagation of secondary senescence.. SASP released by one senescent population can drive neighboring cells toward senescence. If the initiating cells are removed, a positive-feedback loop may therefore be interrupted: fewer senescent cells → less SASP → less induction of new senescence → progressively healthier cellular composition.
Extracellular-matrix remodeling. Matrix proteases and profibrotic/remodeling factors are part of SASP. With their chronic source gone, collagen and other matrix components can slowly be reorganized. My raised lesions becoming flatter and smoother is a visible example of this general phenomenon; comparable remodeling could be happening invisibly in other tissues.
Given this visual evidence, the other changes below become likely rather than merely plausible.
Reduced SASP/inflammaging. Since SASP is able to trigger inflammation and even secondary senescence in cells nearby, eliminating its source may produce effects that persist far longer than the senolytic exposure itself.
Improved endothelial function. Over a period of weeks, endothelial remodeling could plausibly influence vascular elasticity, nitric-oxide biology and microvascular function.
Reduced propagation of secondary senescence.. SASP released by one senescent population can drive neighboring cells toward senescence. If the initiating cells are removed, a positive-feedback loop may therefore be interrupted: fewer senescent cells → less SASP → less induction of new senescence → progressively healthier cellular composition.
Extracellular-matrix remodeling. Matrix proteases and profibrotic/remodeling factors are part of SASP. With their chronic source gone, collagen and other matrix components can slowly be reorganized. My raised lesions becoming flatter and smoother is a visible example of this general phenomenon; comparable remodeling could be happening invisibly in other tissues.