Size and Aging From a Programmed Perspective
Within a given species, larger individuals tend to age faster and die younger. Between species, larger species tend to live longer - though there are many exceptions to this rule. Here is an open access article on this phenomenon from a programmed aging perspective, i.e. the author is building on his hyperfunction theory to say that aging is a genetic program of growth that runs awry to cause damage in old age, past the point at which evolutionary selection guides its operation. This is as opposed to aging as straightforward "wear and tear" type damage that accumulates as a result of the normal operation of metabolism over time, becoming meaningfully harmful only past the age at which evolutionary selection favors further adaptations to reduce, avoid, or repair this damage.
It has been known for millennia that large animals live longer, inspiring numerous theories of aging. For example, elephants and humans live longer than mice, which in turn live longer than worms and flies. The correlation is not perfect, with many explainable exceptions, but it is still obvious. In contrast, within each species (e.g., mice and some other mammals) small body size is associated with longevity and slow aging. The concept that aging (and age-related diseases) is an aimless continuation of developmental growth, a hyperfunction driven by the same nutrient-sensing and growth-promoting pathways such as MTOR, may explain this longstanding paradox.Fast versus slow aging may depend on whether the organism "grows fast" or "develops longer": first case should be associated with high MTOR. Exceptions may be numerous. Small size is not always related to the GH/IGF/MTOR pathway but instead may be caused by defects that shorten life span. But understanding of each exception will further illuminate the rules. On a wider scale (from worm to whale), large animals live longer because aging is quasi-programmed. In contrast, "big" mice live shorter because they grow faster than dwarf mice and growth is driven by the same pathways that drive aging. Fast-growing mice are expected to have over-activation of growth-promoting pathways (either by excessive calorie consumption or due to genetic mutations), which drive aging and age-related diseases later. Cellular hyperfunction is the key feature of aging cell, leading to organismal death. Yet, there are also two other crucial aspects of hyperfunction theory: (a) aging as a quasi-program of developmental growth and (b) both processes are driven by the same growth-promoting-signaling pathways including MTOR.