Proposing a Hyperfunction Theory of Aging

There are a great many theories of aging, and here is another for the pile from a researcher who leans towards aging as genetic programming rather than aging as accumulated damage: "The biological mechanisms at the heart of the aging process are a long-standing mystery. An influential theory has it that aging is the result of an accumulation of molecular damage, caused in particular by reactive oxygen species (ROS) produced by mitochondria. This theory also predicts that processes that protect against oxidative damage (involving detoxification, repair and turnover) protect against aging and increase lifespan. ... However, recent tests of the oxidative damage theory, many using the short-lived nematode worm Caenorhabditis elegans, have often failed to support the theory. This motivates consideration of alternative models. One new theory [proposes] that aging is caused by hyperfunction, i.e. over-activity during adulthood of processes (particularly biosynthetic) that contribute to development and reproduction. Such hyperfunction can lead to hypertrophy-associated pathologies, which cause the age increase in mortality. ... Here we assess whether the hyperfunction theory is at all consistent with what is know about C. elegans aging, and conclude that it is. In particular, during adulthood C. elegans show a number of changes that may reflect pathology and/or hyperfunction. Such changes seem to contribute to mortality, at least in some cases (e.g. yolk accumulation). ... Our assessment suggests that the hyperfunction theory is a plausible alternative to the molecular damage theory to explain aging in C. elegans."



This theory sounds plausible - especially since the concept of "damage" is difficult to define. A lot of development involves rapid destruction of certain tissues - which could be construed as programmed "damage." Also, I believe, some tissue differentiation programs share pathways with apoptosis processes.

This could be a only semantic distinction.
Aside from unambiguous environmentally caused damage (e.g., heat, UV, etc.,) how can we quantify "damage" in differentiated tissue, and be sure it's not a result of a genetic program?

Posted by: Lou Pagnucco at August 10th, 2012 9:33 AM

Aging theory and aging research has been greatly slowed and misdirected over the last fifty years by the dominance of oxidative damage theory which basically holds that aging is essentially outside of the capabilities of natural selection to mitigate its effects. This wrong headed conclusion greatly damaged progress in this field for half a century. Now, theories such as hyperfunction again may be viewed as casting aging beyond the control of natural selection, eliminating the mitigation of aging as a practical possibility. With the fall of the oxidative damage theories of aging, it is now an opportune time to consider theories of aging that are grounded in evolution theory which propose that aging is the result of the action of standard selection forces and therefore open to mitigation.

Conventional aging theories greatly lag the work being done in genetics and stem cell/ developmental biology on mitigation of aging. Theories exist such as "Mate Selection Scale and Aging" // are consistant with evolutionary thought and also provide a conceptual foundation for the experimental work being done.

Posted by: Kevin L Brown at March 11th, 2013 9:39 PM

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