21. What have we learned from aging of model organisms as applied to humans?

We learned that even the best interventions yield marginal lifespan gains in mice, contrasting with radical lifespan extensions in long-lived species, and that the longevity effects in lab settings (e.g. in mice) and in nature (across species) are achieved by different mechanisms. If we are to achieve significant changes in human lifespan in future, we should be thinking multi-species, multi-cell type and multi-modal. We also learned that fundamentals of aging (the essence of aging due to rise in deleteriome) generalize better across species than interventions generalize, whereas no intervention has yet shown robust extension of human lifespan. Targeting damage accumulation in humans has potential, but for this we should better understand differences between short- and long-lived species and cell types, discover how biology operates within thermodynamic constraints while opposing deleterious change, and uncover causal inferences.