Background: Accumulation of various damages is considered the primary cause of aging throughout the history of gerontology. No progress has been made in extending animal lifespan under guidance of this concept. This concept denies existence of longevity genes, but it has been experimentally shown that manipulating genes that affect cell division rates can increase the maximum lifespan of animals. These methods of prolonging life are unsuitable for humans because of dangerous side effects, but they undoubtedly indicate the programed nature of aging.
Objective: The objective was to understand the mechanism of programed aging to determine how to solve the problem of longevity.
Methods: Fundamental research has already explored key details relating to the mechanism of programed aging, but they are scattered across different fields of knowledge. The way was to recognize and combine them into a uniform mechanism.
Results: Only a decrease in bioenergetics is under direct genetic control. This causes many different harmful processes that serve as the execution mechanism of the aging program. The aging rate and, therefore, lifespan are determined by the rate of cell proliferation and the magnitude of the decrease in bioenergetics per cell division in critical tissues.
Conclusion: The mechanism of programed aging points the way to achieving unlimited healthy life: it is necessary to develop a means for managing bioenergetics. More concrete, we have to modify mitochondrial mechanism that controls the [ATP]/[ADP] level. It has already been substantially studied by molecular biologists and is now waiting for researchers from gerontology.