Seven ways not to think carefully about aging

Many experts in the field of biogerontology organize their research plans based on conceptual schemas that are hard to justify, logically problematic, and distracting. These include the ideas: (a) that there is a cause for aging; (b) that each person has a biological age; (c) that published clocks can measure that biological age; (d) that cells have an age; (e) that old cells can rejuvenate and become young again; (f) that biomarkers of age measure rate of aging; (g) that interventions improve either healthspan or lifespan, but not both; and (h) that collections of Hallmarks of aging move the field forward, not backwards. Recognizing the problems and inconsistencies of these very common (though often unconscious) assumptions could help scientists think more clearly and effectively about what to work on. Accumulating data from mouse studies suggest that many or all varieties of slow-aging, long-lived mice, even as young adults, share multiple physiological and molecular traits whose effects may shed light on the pathogenesis of late-life disease, and whose origins may point to new anti-aging interventions. This Comment critiques assumptions and paradigms frequently used in the geroscience field, aiming at enhancing clarity and plausibility of research and conceptual frameworks within and beyond the aging community.