The accumulation of lipofuscin, i.e., indigestible intracellular debris, might be the main cause of age-related diseases that we see today. However, without being able to replace mutated mitochondrial DNA (mtDNA) and damaged and mutated nuclear DNA (nDNA), we will still eventually succumb to aging. Thus, we must save copies of mitochondrial and nuclear DNA at as young an age as possible, or at least from cell types with the lowest rates of mutation. MtDNA has a 10-100x higher rate of mutation than nDNA, as mitochondria are sites of free radical production. We may need to replace mtDNA before damaged and mutated nDNA. If so, we will need a strategy to deliver pristine mtDNA to cells around the the body and destroy the old mtDNA. A strategy for doing so is described herein.