Theorists agree that living organisms possess extensive maintenance and repair functions that act to repair damage. This is a major and obvious difference between living organisms and non-living entities and a main reason that the generic wear and tear theories do not work. As a result, there now exist both programmed and non-programmed theories of aging based on maintenance and repair functions.
Maintenance and Repair Functions
Here are examples of known maintenance and repair functions:
Claws, nails, hair, and fur grow to replace worn items.
Dead cells are replaced. Some cells (e.g. epithelial cells) only last a short time (weeks).
Certain forms of molecular damage (e.g. telomere shortening) are repaired.
Non-Programmed Maintenance Theories of Aging
According to traditional evolutionary mechanics theory, an organism cannot evolve a mechanism whose primary purpose is to limit life span but can evolve maintenance mechanisms whose purpose is to extend life span. Because of Medawar's hypothesis, organisms do not need life spans longer than some multiple of their age of sexual maturity and therefore there is little or no evolutionary motivation towards developing and retaining maintenance mechanisms capable of delaying deterioration beyond that point.
Different manifestations of aging appear to be caused by greatly different mechanisms. Much heart disease is caused by buildup of artery deposits. Cancer appears to be caused by molecular changes that cause uncontrolled cell growth. These mechanisms are very different leading to the conclusion that different maintenance and repair mechanisms are involved in repair of damage leading to various different manifestations. This leads to the idea that a number (potentially a large number) of different maintenance mechanisms evolved independently. If an animal species was troubled by excessively early heart disease it would evolve better anti-heart disease mechanisms. If cancer became a problem, it would evolve a better anti-cancer mechanism and so forth. Non-programmed maintenance theories suggest that in each species, the various maintenance mechanisms have each been tailored by the evolution process to that species' need for life span. In a short-lived species, all of the maintenance functions are somehow less effective and therefore unrepaired damage accumulates more rapidly than in a longer-lived species.
PROS: Compatible with traditional evolutionary mechanics theory. CONS: Major problems explaining experimental observations.
Programmed Maintenance Theories of Aging
According to alternative evolutionary mechanics theories and associated aging theories, an organism can evolve both anti-aging functions necessary to achieve a life span loosely based on Medawar's criteria, and a life span regulation mechanism necessary to limit life span to a species-specific value also loosely based on Medawar's criteria. A life span exceeding the optimum life span for the species creates evolutionary disadvantage. Therefore, assuming the same sorts of maintenance functions described above, the combined system could be as described below. In this concept a biological life span regulation function purposely discontinues or slows maintenance functions at a species-unique age. Like most evolved biological functions, the proposed regulation mechanism is capable of adapting (within a genetically designed range) to local or temporary conditions via sense functions. In this concept the major difference between mammal species is in the control (clock, sense, signaling) mechanism as opposed to differences in each of the maintenance mechanisms.
A major feature of this concept is the existence of mechanisms that are common to multiple manifestations of aging including clock, sensory, and signaling functions. This contrasts with the non-programmed concept of independent maintenance functions and has major medical implications.
PROS: Excellent fit with experimental evidence. CONS: Incompatible with traditional evolutionary mechanics theory; requires an alternative mechanics theory.
Observational Evidence Favoring Programmed Maintenance Aging Theories
Progeria and Werner Syndrome: These human conditions accelerate many or most manifestations of aging. That a single-gene malfunction affects multiple manifestations suggests commonality between causes, which fits programmed theory but not independent maintenance mechanisms.
Caloric Restriction and Stress Response: Programmed theories suggest that there would be benefit to a life span regulation mechanism that responded to these temporary conditions by adjusting life span. The suggested programmed mechanism matches observations. These observations are essentially incompatible with the non-programmed theory.
Common Aging Manifestations: Even though there is a 100:1 range in mammal life spans, manifestations of aging are remarkably similar between mammal species. It seems implausible that this would be the case in the non-programmed scenario.
Short-term Nature of Maintenance: The example maintenance functions are short-term and operate over periods of weeks or months. The maintenance necessary for all of the major manifestations of aging is also short-term. If it was not, short-lived animals would not display some of the manifestations. This is a difficulty for the non-programmed theory: Why would a function that successfully held off cancer between mouse age and cat age in the cat fail to achieve human life span in the cat?
Rapid Adaptation: If one assumes that a species-specific design-limited life span has merit then the life span regulation mechanism concept is clearly superior in that it can adjust rapidly to a species' adaptive need for shorter or longer life span. All of the maintenance functions can be adjusted by altering a few genes or even single gene associated with the control mechanism.
Aging Genes: The finding that a single gene can significantly affect life span suggests commonality.
Non-Aging Species: Instances of negligible senescence suggest that nearly perfect maintenance is possible.
Digital Genetics: The digital nature of genetics data imposes limits on the degree of variability possible in any parameter. In a digital system nothing is indefinitely variable. This makes it difficult to imagine the sort of continuous variation in maintenance mechanisms necessary to explain multi-species observations in the non-programmed case. Would we need a 99 percent effective anti-cancer mechanism in rats, a 99.9 percent effective mechanism in cats, perhaps 99.99 percent effective in humans and what, 99.9999 percent in negligibly senescent species? How would each of the maintenance mechanisms actually differ from species to species in order to produce the observed effects? This is not a problem for the programmed mechanism.
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